Materiały źródłowe

• #1 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  Asthma is a common chronic disease worldwide and affects approximately 25 million persons in the United States. The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. […] The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. […] The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

• #2 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  Asthma is a chronic inflammatory disorder of the airways. This feature of asthma has implications for the diagnosis, management, and potential prevention of the disease. […] Airway inflammation contributes to airway hyperresponsiveness, airflow limitation, respiratory symptoms, and disease chronicity. […] Gene-by-environment interactions are important to the expression of asthma. […] The concepts underlying asthma pathogenesis have evolved dramatically in the past 25 years and are still undergoing evaluation as various phenotypes of this disease are defined and greater insight links clinical features of asthma with genetic patterns. […] Central to the various phenotypic patterns of asthma is the presence of underlying airway inflammation, which is variable and has distinct but overlapping patterns that reflect different aspects of the disease, such as intermittent versus persistent or acute versus chronic manifestations.

• #3 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #4 Eighty-eight variants highlight the role of T cell regulation and airway remodeling in asthma pathogenesis | Nature Communications

  https://www.nature.com/articles/s41467-019-14144-8

  Asthma is one of the most common chronic diseases affecting both children and adults. […] Our results increase the number of asthma variants and implicate genes with known role in T cell regulation, inflammation and airway remodeling in asthma pathogenesis. […] T2 high asthma is characterized by increased activation of T helper cells of type 2 (Th2), innate lymphoid cells of type 2 (ILC2), and eosinophils. […] Together, the TGFBR1 3 prime UTR variant rs41283642_T described above and rs117683492_A at the SMAD3 locus point to increased risk of asthma in individuals with defective TGFR1 signaling in line with its known role in immunosuppression. […] The results highlight the role of Th cells in asthma in line with imbalanced T cell regulation reported to play a critical role in asthma pathogenesis.

• #5 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  The concept that asthma may be a continuum of these processes that can lead to moderate and severe persistent disease is of critical importance to understanding the pathogenesis, pathophysiology, and natural history of this disease. […] Inflammation has a central role in the pathophysiology of asthma. […] The processes by which these interactive events occur and lead to clinical asthma are still under investigation. […] The pattern of airway inflammation in asthma, however, does not necessarily vary depending upon disease severity, persistence, and duration of disease. […] The mechanisms involved have yet to be established and may include enhanced generation of pro-inflammatory cytokines. […] The mechanisms influencing airway hyperresponsiveness are multiple and include inflammation, dysfunctional neuroregulation, and structural changes; inflammation appears to be a major factor in determining the degree of airway hyperresponsiveness.

• #6 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Asthma is a heterogeneous lung disease with variable phenotypes (clinical presentations) and distinctive endotypes (mechanisms). Over the last decade, considerable efforts have been made to dissect the cellular and molecular mechanisms of asthma. Aberrant T helper type 2 (Th2) inflammation is the most important pathological process for asthma, which is mediated by Th2 cytokines, such as interleukin (IL)-5, IL-4, and IL-13. Approximately 50% of mild-to-moderate asthma and a large portion of severe asthma is induced by Th2-dependent inflammation. Th2-low asthma can be mediated by non-Th2 cytokines, including IL-17 and tumor necrosis factor-α. There is emerging evidence to demonstrate that inflammation-independent processes also contribute to asthma pathogenesis. […] The pathological mechanisms of asthma are complex, varying in different phenotypes caused by different environmental triggers, ages, obesity, genetic factors, etc. In addition to airway inflammation, there is emerging evidence to suggest that inflammation-independent processes also contribute to asthma pathogenesis.

• #7 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Asthma is a heterogeneous lung disease with variable phenotypes (clinical presentations) and distinctive endotypes (mechanisms). Over the last decade, considerable efforts have been made to dissect the cellular and molecular mechanisms of asthma. Aberrant T helper type 2 (Th2) inflammation is the most important pathological process for asthma, which is mediated by Th2 cytokines, such as interleukin (IL)-5, IL-4, and IL-13. Approximately 50% of mild-to-moderate asthma and a large portion of severe asthma is induced by Th2-dependent inflammation. Th2-low asthma can be mediated by non-Th2 cytokines, including IL-17 and tumor necrosis factor-α. There is emerging evidence to demonstrate that inflammation-independent processes also contribute to asthma pathogenesis. […] The pathological mechanisms of asthma are complex, varying in different phenotypes caused by different environmental triggers, ages, obesity, genetic factors, etc. In addition to airway inflammation, there is emerging evidence to suggest that inflammation-independent processes also contribute to asthma pathogenesis.

• #8 Pathogenesis of atopic asthma – GPnotebook

  https://gpnotebook.com/en-GB/pages/respiratory-and-chest-medicine/asthma/pathogenesis-of-atopic-asthma

  Atopic asthma is the result of airway inflammation caused by exposure to an environmental allergen. […] Patients with asthma have an exuberant Th2-mediated IgE humoural immune response. […] IgE binds to bronchial mast cells via the FcERI (high affinity receptor) resulting in degranulation and the release of pro-inflammatory mediators. […] There are two phases of inflammation: acute phase and delayed phase. […] The results of inflammation are: bronchial hyper-reactivity, symptoms of cough, wheeze and chest tightness, signs of variable polyphonic wheezes.

• #9 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. […] Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease. […] Airway inflammation in asthma may represent a loss of normal balance between two „opposing” populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation.

• #10 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Th2 inflammation has two major phases: 1. Sensitization: When allergens enter the low airways, antigen-presenting cells process and present the allergens to Th2 cells, which secret Th2 cytokines, including IL-5, IL-4, and IL-13. 2. Challenge: When the same allergens enter the airways, they bind to IgE, which induces mast cells to release mediators, such as leukotrienes (LTs), histamine, and ILs. In addition, IL-5 facilitates eosinophil production, maturation, and recruitment to the lungs. Eosinophils also release mediators, including major basic protein (MBP), which stimulates mast cells to release histamines and LTs. […] Recent studies demonstrated that the airway epithelium produces cytokines in response to injury, infection, and pollutants. These epithelial-derived cytokines include thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. TSLP, IL-25, and IL-33 activate type 2 innate lymphoid cells (ILC2), which generate Th2 cytokines, such as IL-5 and IL-13 and induce Th2 lung inflammation.

• #11 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Th2 inflammation has two major phases: 1. Sensitization: When allergens enter the low airways, antigen-presenting cells process and present the allergens to Th2 cells, which secret Th2 cytokines, including IL-5, IL-4, and IL-13. 2. Challenge: When the same allergens enter the airways, they bind to IgE, which induces mast cells to release mediators, such as leukotrienes (LTs), histamine, and ILs. In addition, IL-5 facilitates eosinophil production, maturation, and recruitment to the lungs. Eosinophils also release mediators, including major basic protein (MBP), which stimulates mast cells to release histamines and LTs. […] Recent studies demonstrated that the airway epithelium produces cytokines in response to injury, infection, and pollutants. These epithelial-derived cytokines include thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. TSLP, IL-25, and IL-33 activate type 2 innate lymphoid cells (ILC2), which generate Th2 cytokines, such as IL-5 and IL-13 and induce Th2 lung inflammation.

• #12 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #13 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #14 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Th2 lymphocytes play an integral role where they produce a series of interleukins (IL-4, IL-5, IL-13) and GM-CSF, which aid in communication with other cells and sustain inflammation. […] Within the next several hours, the late phase occurs, in which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. […] It is critical to recognize both of these two mechanisms to target therapy and relieve both bronchoconstriction and inflammation, depending on the severity of the disease. […] Airway hyperresponsiveness is a crucial feature of asthma; this is an exaggerated bronchoconstrictor response, usually to different stimuli. […] There are a variety of mechanisms leading to airway hyperresponsiveness.

• #15 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Th2 lymphocytes play an integral role where they produce a series of interleukins (IL-4, IL-5, IL-13) and GM-CSF, which aid in communication with other cells and sustain inflammation. […] Within the next several hours, the late phase occurs, in which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. […] It is critical to recognize both of these two mechanisms to target therapy and relieve both bronchoconstriction and inflammation, depending on the severity of the disease. […] Airway hyperresponsiveness is a crucial feature of asthma; this is an exaggerated bronchoconstrictor response, usually to different stimuli. […] There are a variety of mechanisms leading to airway hyperresponsiveness.

• #16 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Th2 lymphocytes play an integral role where they produce a series of interleukins (IL-4, IL-5, IL-13) and GM-CSF, which aid in communication with other cells and sustain inflammation. […] Within the next several hours, the late phase occurs, in which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. […] It is critical to recognize both of these two mechanisms to target therapy and relieve both bronchoconstriction and inflammation, depending on the severity of the disease. […] Airway hyperresponsiveness is a crucial feature of asthma; this is an exaggerated bronchoconstrictor response, usually to different stimuli. […] There are a variety of mechanisms leading to airway hyperresponsiveness.

• #17 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Th2 inflammation has two major phases: 1. Sensitization: When allergens enter the low airways, antigen-presenting cells process and present the allergens to Th2 cells, which secret Th2 cytokines, including IL-5, IL-4, and IL-13. 2. Challenge: When the same allergens enter the airways, they bind to IgE, which induces mast cells to release mediators, such as leukotrienes (LTs), histamine, and ILs. In addition, IL-5 facilitates eosinophil production, maturation, and recruitment to the lungs. Eosinophils also release mediators, including major basic protein (MBP), which stimulates mast cells to release histamines and LTs. […] Recent studies demonstrated that the airway epithelium produces cytokines in response to injury, infection, and pollutants. These epithelial-derived cytokines include thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. TSLP, IL-25, and IL-33 activate type 2 innate lymphoid cells (ILC2), which generate Th2 cytokines, such as IL-5 and IL-13 and induce Th2 lung inflammation.

• #18 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Th2 inflammation has two major phases: 1. Sensitization: When allergens enter the low airways, antigen-presenting cells process and present the allergens to Th2 cells, which secret Th2 cytokines, including IL-5, IL-4, and IL-13. 2. Challenge: When the same allergens enter the airways, they bind to IgE, which induces mast cells to release mediators, such as leukotrienes (LTs), histamine, and ILs. In addition, IL-5 facilitates eosinophil production, maturation, and recruitment to the lungs. Eosinophils also release mediators, including major basic protein (MBP), which stimulates mast cells to release histamines and LTs. […] Recent studies demonstrated that the airway epithelium produces cytokines in response to injury, infection, and pollutants. These epithelial-derived cytokines include thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. TSLP, IL-25, and IL-33 activate type 2 innate lymphoid cells (ILC2), which generate Th2 cytokines, such as IL-5 and IL-13 and induce Th2 lung inflammation.

• #19 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  Eosinophils are granulocytes in blood produced in the bone marrow with other white blood cells making about 13% of white blood cells. Eosinophil plays multiple functions and is an important component of allergic and asthmatic type 2 immune responses. […] During asthma attack, eosinophils are stimulated to release proteins from granules including major basic protein, eosinophil peroxidase, eosinophil cationic protein, and eosinophil-derived neurotoxin, all of which are toxic to the epithelial cells of airway. […] Eosinophils control the allergen-dependent Th2 pulmonary immune responses activated by dendritic cells and T cells as well as decrease Th1 responses. […] Although various bioactive proteins such as IL-3 and granulocyte-macrophage colony-stimulating factor affect the life cycle of eosinophils, eosinophils react mainly to IL-5.

• #20 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  The key function of IL-5 in tissues is to stimulate the growth, recruitment, activation, and differentiation of eosinophils. […] IL-5 can also promote eosinophilic infiltration in bronchial airways due to synergetic effect of IL-5 with other chemoattractants of eosinophils such as eotaxins. […] IL-33 is the newly discovered member of cytokine of IL-1 group. […] Mast cells are the source of the Th2 cytokines including IL-4 and IL-5 that regulate antibodies class switching to IgE and eosinophil production, respectively. […] Type 2 innate lymphoid cells (ILC2) are non-B/non-T cells that release IL-5 and IL-13 on activation by IL-25 and IL-33 and expressed MHC class II high and CD11cdull on their surface.

• #21 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  The key function of IL-5 in tissues is to stimulate the growth, recruitment, activation, and differentiation of eosinophils. […] IL-5 can also promote eosinophilic infiltration in bronchial airways due to synergetic effect of IL-5 with other chemoattractants of eosinophils such as eotaxins. […] IL-33 is the newly discovered member of cytokine of IL-1 group. […] Mast cells are the source of the Th2 cytokines including IL-4 and IL-5 that regulate antibodies class switching to IgE and eosinophil production, respectively. […] Type 2 innate lymphoid cells (ILC2) are non-B/non-T cells that release IL-5 and IL-13 on activation by IL-25 and IL-33 and expressed MHC class II high and CD11cdull on their surface.

• #22 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Th2 lymphocytes play an integral role where they produce a series of interleukins (IL-4, IL-5, IL-13) and GM-CSF, which aid in communication with other cells and sustain inflammation. […] Within the next several hours, the late phase occurs, in which eosinophils, basophils, neutrophils, and helper and memory T-cells all localize to the lungs as well, which perform bronchoconstriction and cause inflammation. […] It is critical to recognize both of these two mechanisms to target therapy and relieve both bronchoconstriction and inflammation, depending on the severity of the disease. […] Airway hyperresponsiveness is a crucial feature of asthma; this is an exaggerated bronchoconstrictor response, usually to different stimuli. […] There are a variety of mechanisms leading to airway hyperresponsiveness.

• #23 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  Asthma is a common chronic disease worldwide and affects approximately 25 million persons in the United States. The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. […] The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. […] The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

• #24 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  Asthma is a common chronic disease worldwide and affects approximately 25 million persons in the United States. The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. […] The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. […] The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

• #25 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  Asthma is a common chronic disease worldwide and affects approximately 25 million persons in the United States. The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. […] The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. […] The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

• #26 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #27 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #28 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #29 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #30 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #31 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  To assess airway hyperresponsiveness, bronchial provocation tests are used to determine the severity. […] Therefore, targeted treatment can be employed early to combat asthma and hyperresponsiveness. […] A person can have irreversible obstruction of airflow, which is believed to be due to airway remodeling. […] Remodeling occurs by epithelial cells transitioning to mesenchymal, increasing the smooth muscle content. […] Additionally, eosinophils can further exacerbate airway remodeling due to their release of TGF-B and cytokines by interactions with mast cells. These mechanisms of airway remodeling may worsen inflammation and aggravate asthma over time if not treated and managed correctly.

• #32 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. […] Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease. […] Airway inflammation in asthma may represent a loss of normal balance between two „opposing” populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation.

• #33 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. […] Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease. […] Airway inflammation in asthma may represent a loss of normal balance between two „opposing” populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation.

• #34 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  Airway remodeling involves an activation of many of the structural cells, with consequent permanent changes in the airway that increase airflow obstruction and airway responsiveness and render the patient less responsive to therapy. […] The development of monoclonal antibodies against IgE has shown that the reduction of IgE is effective in asthma treatment. […] The role of genetics in IgE production, airway hyperresponsiveness, and dysfunctional regulation of the generation of inflammatory mediators has appropriately captured much attention. […] The influence of viral respiratory infections on the development of asthma may depend on an interaction with atopy. […] In summary, our understanding of asthma pathogenesis and underlying mechanisms now includes the concept that gene-by-environmental interactions are critical factors in the development of airway inflammation and eventual alteration in the pulmonary physiology that is characteristic of clinical asthma.

• #35 Bronchial Asthma: Etiology, Pathophysiology, Diagnosis and Management

  https://austinpublishinggroup.com/pulmonary-respiratory-medicine/fulltext/ajprm-v9-id1085.php

  Bronchial asthma is a chronic inflammatory disease of the respiratory passages, occurring with the participation of mast cells, eosinophils and T-lymphocytes, the release of a large number of inflammatory mediators. […] The main pathophysiological characteristics of asthma are inflammation and airway remodeling, which include goblet cell hyperplasia, subepithelial fibrosis, collagen deposition, mucosal gland, hyperplasia, smooth muscle hypertrophy, and changes in the extracellular matrix. These changes can result in immune system imbalance, eventually leading to airway hyperresponsiveness. […] Long-standing inflammation will damage airways, and induces airway remodelling, entailing subepithelial fibrosis under the basement membrane, smooth muscle hypertrophy, and submucosal gland hyperplasia. This results in intractable asthma, presenting irreversible airflow limitation and persistent airway hyperresponsiveness.

• #36 Bronchial Asthma: Etiology, Pathophysiology, Diagnosis and Management

  https://austinpublishinggroup.com/pulmonary-respiratory-medicine/fulltext/ajprm-v9-id1085.php

  Bronchial asthma is a chronic inflammatory disease of the respiratory passages, occurring with the participation of mast cells, eosinophils and T-lymphocytes, the release of a large number of inflammatory mediators. […] The main pathophysiological characteristics of asthma are inflammation and airway remodeling, which include goblet cell hyperplasia, subepithelial fibrosis, collagen deposition, mucosal gland, hyperplasia, smooth muscle hypertrophy, and changes in the extracellular matrix. These changes can result in immune system imbalance, eventually leading to airway hyperresponsiveness. […] Long-standing inflammation will damage airways, and induces airway remodelling, entailing subepithelial fibrosis under the basement membrane, smooth muscle hypertrophy, and submucosal gland hyperplasia. This results in intractable asthma, presenting irreversible airflow limitation and persistent airway hyperresponsiveness.

• #37 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The current „hygiene hypothesis” of asthma illustrates how this cytokine imbalance may explain some of the dramatic increases in asthma prevalence in westernized countries. […] Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. […] Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. […] Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation.

• #38 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The current „hygiene hypothesis” of asthma illustrates how this cytokine imbalance may explain some of the dramatic increases in asthma prevalence in westernized countries. […] Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. […] Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. […] Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation.

• #39 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The current „hygiene hypothesis” of asthma illustrates how this cytokine imbalance may explain some of the dramatic increases in asthma prevalence in westernized countries. […] Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. […] Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. […] Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation.

• #40 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #41 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #42 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  Eosinophilic asthma is known as a main phenotype of asthma classified on the basis of immune cells involved in inflammatory response in the respiratory airway. […] Different cells and cytokines are involved in its pathogenesis including eosinophil, mast cells, type 2 helper T cells, innate lymphoid cells, IL-4, IL-5, and IL-13. […] Eosinophilic airway inflammation is the main pathophysiological mechanism of eosinophilic asthma. Eosinophilic asthma develops from complex immunologic and pro-inflammatory mechanisms, mainly driven by T helper 2 (Th2) cells, which is a part of adaptive immunity release interleukins (IL-5, IL-4, and IL-13). […] As a result, airway eosinophilia arises due to the biological activity of both type 2 helper T (Th2) and type 2 innate lymphoid (ILC2) cells, which are critically participating in the pathogenic process of type-2 inflammation in eosinophilic allergic and nonallergic asthma.

• #43 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  Eosinophilic asthma is known as a main phenotype of asthma classified on the basis of immune cells involved in inflammatory response in the respiratory airway. […] Different cells and cytokines are involved in its pathogenesis including eosinophil, mast cells, type 2 helper T cells, innate lymphoid cells, IL-4, IL-5, and IL-13. […] Eosinophilic airway inflammation is the main pathophysiological mechanism of eosinophilic asthma. Eosinophilic asthma develops from complex immunologic and pro-inflammatory mechanisms, mainly driven by T helper 2 (Th2) cells, which is a part of adaptive immunity release interleukins (IL-5, IL-4, and IL-13). […] As a result, airway eosinophilia arises due to the biological activity of both type 2 helper T (Th2) and type 2 innate lymphoid (ILC2) cells, which are critically participating in the pathogenic process of type-2 inflammation in eosinophilic allergic and nonallergic asthma.

• #44 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  Eosinophilic asthma is known as a main phenotype of asthma classified on the basis of immune cells involved in inflammatory response in the respiratory airway. […] Different cells and cytokines are involved in its pathogenesis including eosinophil, mast cells, type 2 helper T cells, innate lymphoid cells, IL-4, IL-5, and IL-13. […] Eosinophilic airway inflammation is the main pathophysiological mechanism of eosinophilic asthma. Eosinophilic asthma develops from complex immunologic and pro-inflammatory mechanisms, mainly driven by T helper 2 (Th2) cells, which is a part of adaptive immunity release interleukins (IL-5, IL-4, and IL-13). […] As a result, airway eosinophilia arises due to the biological activity of both type 2 helper T (Th2) and type 2 innate lymphoid (ILC2) cells, which are critically participating in the pathogenic process of type-2 inflammation in eosinophilic allergic and nonallergic asthma.

• #45 Eosinophilic Asthma | IntechOpen

  https://www.intechopen.com/chapters/67117

  Eosinophilic asthma is known as a main phenotype of asthma classified on the basis of immune cells involved in inflammatory response in the respiratory airway. […] Different cells and cytokines are involved in its pathogenesis including eosinophil, mast cells, type 2 helper T cells, innate lymphoid cells, IL-4, IL-5, and IL-13. […] Eosinophilic airway inflammation is the main pathophysiological mechanism of eosinophilic asthma. Eosinophilic asthma develops from complex immunologic and pro-inflammatory mechanisms, mainly driven by T helper 2 (Th2) cells, which is a part of adaptive immunity release interleukins (IL-5, IL-4, and IL-13). […] As a result, airway eosinophilia arises due to the biological activity of both type 2 helper T (Th2) and type 2 innate lymphoid (ILC2) cells, which are critically participating in the pathogenic process of type-2 inflammation in eosinophilic allergic and nonallergic asthma.

• #46 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  Asthma is a heterogeneous lung disease with variable phenotypes (clinical presentations) and distinctive endotypes (mechanisms). Over the last decade, considerable efforts have been made to dissect the cellular and molecular mechanisms of asthma. Aberrant T helper type 2 (Th2) inflammation is the most important pathological process for asthma, which is mediated by Th2 cytokines, such as interleukin (IL)-5, IL-4, and IL-13. Approximately 50% of mild-to-moderate asthma and a large portion of severe asthma is induced by Th2-dependent inflammation. Th2-low asthma can be mediated by non-Th2 cytokines, including IL-17 and tumor necrosis factor-α. There is emerging evidence to demonstrate that inflammation-independent processes also contribute to asthma pathogenesis. […] The pathological mechanisms of asthma are complex, varying in different phenotypes caused by different environmental triggers, ages, obesity, genetic factors, etc. In addition to airway inflammation, there is emerging evidence to suggest that inflammation-independent processes also contribute to asthma pathogenesis.

• #47 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #48 Targeting cell signaling in allergic asthma | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-019-0079-0

  Several therapeutics have been introduced to interfere with the IL-4/IL-13/JAK/STAT-6 pathway. These include inhibitors of JAK, dimerization suppressors, phosphopeptides targeting the SH2 domain of STAT-6, decoy oligonucleotides, siRNAs, and finally synthetic small molecules. […] The Th2-high subtype is characterized by marked eosinophilic infiltration of the airways, whereas the Th2-low subtype is characterized by neutrophilic infiltration. […] The receptors of allergic cytokines, including IL-4, IL-5, IL-13, IL-31, and thymic stromal lymphopoietin (TSLP), trigger the JAK/STAT pathway. This is the main route involved in the pathogenesis of asthma. […] The activation of the Wnt signaling pathway was also shown to accelerate the proliferation of airway smooth muscle cells, which are involved in airway remodeling.

• #49 Occupational asthma: Pathogenesis – UpToDate

  https://www.uptodate.com/contents/occupational-asthma-pathogenesis

  Occupational asthma is a type of work-related asthma that is caused by immunologic (identified or presumed) and nonimmunologic stimuli present in the workplace. […] The pathogenesis and pathology of occupational asthma will be reviewed here. […] Two main types of occupational asthma have been recognized: Immunologically-mediated. This type includes immunoglobulin E (IgE) and non-IgE-mediated responses following chronic exposure and respiratory sensitization to high or low molecular weight agents. […] Nonimmunologic, irritant-mediated, also called irritant-induced asthma. This type includes reactive airways dysfunction syndrome (RADS) caused by a single high-level exposure to an irritant, irritant-induced asthma caused by multiple high-level exposures to an irritant, and possibly asthma caused by chronic lower level of exposure, although the latter is controversial.

• #50 Occupational asthma: Pathogenesis – UpToDate

  https://www.uptodate.com/contents/occupational-asthma-pathogenesis

  Occupational asthma is a type of work-related asthma that is caused by immunologic (identified or presumed) and nonimmunologic stimuli present in the workplace. […] The pathogenesis and pathology of occupational asthma will be reviewed here. […] Two main types of occupational asthma have been recognized: Immunologically-mediated. This type includes immunoglobulin E (IgE) and non-IgE-mediated responses following chronic exposure and respiratory sensitization to high or low molecular weight agents. […] Nonimmunologic, irritant-mediated, also called irritant-induced asthma. This type includes reactive airways dysfunction syndrome (RADS) caused by a single high-level exposure to an irritant, irritant-induced asthma caused by multiple high-level exposures to an irritant, and possibly asthma caused by chronic lower level of exposure, although the latter is controversial.

• #51 Occupational asthma: Pathogenesis – UpToDate

  https://www.uptodate.com/contents/occupational-asthma-pathogenesis

  Occupational asthma is a type of work-related asthma that is caused by immunologic (identified or presumed) and nonimmunologic stimuli present in the workplace. […] The pathogenesis and pathology of occupational asthma will be reviewed here. […] Two main types of occupational asthma have been recognized: Immunologically-mediated. This type includes immunoglobulin E (IgE) and non-IgE-mediated responses following chronic exposure and respiratory sensitization to high or low molecular weight agents. […] Nonimmunologic, irritant-mediated, also called irritant-induced asthma. This type includes reactive airways dysfunction syndrome (RADS) caused by a single high-level exposure to an irritant, irritant-induced asthma caused by multiple high-level exposures to an irritant, and possibly asthma caused by chronic lower level of exposure, although the latter is controversial.

• #52 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #53 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #54 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #55 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #56 Current Understanding of Asthma Pathogenesis and Biomarkers

  https://www.mdpi.com/2073-4409/11/17/2764

  However, there is accumulating evidence to suggest that inflammation-independent processes are also associated with asthma progression. For instance, recent studies demonstrate that protein kinases, adapter proteins, and other molecules contribute to asthma pathogenesis. […] c-Abl (Abelson tyrosine kinase, Abl, ABL1) is a non-receptor tyrosine kinase that participates in the regulation of smooth muscle contraction, migration, and proliferation. […] These results suggest that c-Abl is a Th2-regulatory protein rather than a Th2-dependent protein. […] The role of periostin in asthma is still under investigation. There are reports to suggest that periostin supports adhesion and migration of IL-5-stimulated human eosinophils and Th2 inflammation in asthma. […] In Th2-low asthma, IL-17 and TNF-α promote the recruitment of neutrophils to the lungs. Protein kinases, adapter protein, miRs, ORMDL3, and gasdermin B are newly identified molecules that contribute to asthma pathogenesis, independent of inflammation.

• #57 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #58 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #59 Pathophysiology Of Asthma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK551579/

  Asthma is becoming a more prevalent disease since the early 1990s. […] There are mechanisms of the phenotype of asthma that has a strong correlation of being inherited, but the mechanism is more complex, as asthma does not follow a Mendelian pattern. Asthma is most likely transmitted by multiple genes, with some variation of locus heterogeneity and polygenic inheritance leading to asthma expression being multifaceted. Atopy or IgE antibodies attack specific antigens or pollutants, which can contribute to the disease. […] There are two phases of an asthma exacerbation, which include the early phase and the late phase. The early phase is initiated by IgE antibodies that are sensitized and released by plasma cells. […] Released from mast cells are histamine, prostaglandins, and leukotrienes. These cells, in turn, contract the smooth muscle and cause airway tightening.

• #60 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  Airway remodeling involves an activation of many of the structural cells, with consequent permanent changes in the airway that increase airflow obstruction and airway responsiveness and render the patient less responsive to therapy. […] The development of monoclonal antibodies against IgE has shown that the reduction of IgE is effective in asthma treatment. […] The role of genetics in IgE production, airway hyperresponsiveness, and dysfunctional regulation of the generation of inflammatory mediators has appropriately captured much attention. […] The influence of viral respiratory infections on the development of asthma may depend on an interaction with atopy. […] In summary, our understanding of asthma pathogenesis and underlying mechanisms now includes the concept that gene-by-environmental interactions are critical factors in the development of airway inflammation and eventual alteration in the pulmonary physiology that is characteristic of clinical asthma.

• #61 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  Airway remodeling involves an activation of many of the structural cells, with consequent permanent changes in the airway that increase airflow obstruction and airway responsiveness and render the patient less responsive to therapy. […] The development of monoclonal antibodies against IgE has shown that the reduction of IgE is effective in asthma treatment. […] The role of genetics in IgE production, airway hyperresponsiveness, and dysfunctional regulation of the generation of inflammatory mediators has appropriately captured much attention. […] The influence of viral respiratory infections on the development of asthma may depend on an interaction with atopy. […] In summary, our understanding of asthma pathogenesis and underlying mechanisms now includes the concept that gene-by-environmental interactions are critical factors in the development of airway inflammation and eventual alteration in the pulmonary physiology that is characteristic of clinical asthma.

• #62 Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma – Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK7223/

  Airway remodeling involves an activation of many of the structural cells, with consequent permanent changes in the airway that increase airflow obstruction and airway responsiveness and render the patient less responsive to therapy. […] The development of monoclonal antibodies against IgE has shown that the reduction of IgE is effective in asthma treatment. […] The role of genetics in IgE production, airway hyperresponsiveness, and dysfunctional regulation of the generation of inflammatory mediators has appropriately captured much attention. […] The influence of viral respiratory infections on the development of asthma may depend on an interaction with atopy. […] In summary, our understanding of asthma pathogenesis and underlying mechanisms now includes the concept that gene-by-environmental interactions are critical factors in the development of airway inflammation and eventual alteration in the pulmonary physiology that is characteristic of clinical asthma.

• #63 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #64 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #65 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #66 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #67 Pathophysiology of asthma – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_asthma

  The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. […] In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma. […] In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors. Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergies.

• #68 Pathophysiology of asthma – Wikipedia

  https://en.wikipedia.org/wiki/Pathophysiology_of_asthma

  The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. […] In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma. […] In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors. Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergies.

• #69 Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/296301-overview

  The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. […] Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease. […] Airway inflammation in asthma may represent a loss of normal balance between two „opposing” populations of Th lymphocytes. Two types of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and IFN-, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation.

• #70 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  The role of bacterial airway colonisation in chronic stable asthma is unclear. However, there is increasing evidence for the role of bacterial pathogen-associated molecular patterns such as lipopolysaccharide in the activation of the innate immune system, which may lead to the expression of a neutrophilic asthma phenotype. […] Airway colonisation with potentially pathogenic bacteria is a common feature of severe asthma and is associated with a neutrophilic phenotype of airways inflammation. […] Mast cells play an important role in the pathogenesis of asthma. […] A defining feature of asthma is the presence of mast cells within the airway smooth muscle (ASM). […] These activated, histamine-depleted HLMC are still able to release equivalent amounts of histamine following IgE-dependent activation indicating that they can still respond to allergen inhalation.

• #71 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  The role of bacterial airway colonisation in chronic stable asthma is unclear. However, there is increasing evidence for the role of bacterial pathogen-associated molecular patterns such as lipopolysaccharide in the activation of the innate immune system, which may lead to the expression of a neutrophilic asthma phenotype. […] Airway colonisation with potentially pathogenic bacteria is a common feature of severe asthma and is associated with a neutrophilic phenotype of airways inflammation. […] Mast cells play an important role in the pathogenesis of asthma. […] A defining feature of asthma is the presence of mast cells within the airway smooth muscle (ASM). […] These activated, histamine-depleted HLMC are still able to release equivalent amounts of histamine following IgE-dependent activation indicating that they can still respond to allergen inhalation.

• #72 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  The role of bacterial airway colonisation in chronic stable asthma is unclear. However, there is increasing evidence for the role of bacterial pathogen-associated molecular patterns such as lipopolysaccharide in the activation of the innate immune system, which may lead to the expression of a neutrophilic asthma phenotype. […] Airway colonisation with potentially pathogenic bacteria is a common feature of severe asthma and is associated with a neutrophilic phenotype of airways inflammation. […] Mast cells play an important role in the pathogenesis of asthma. […] A defining feature of asthma is the presence of mast cells within the airway smooth muscle (ASM). […] These activated, histamine-depleted HLMC are still able to release equivalent amounts of histamine following IgE-dependent activation indicating that they can still respond to allergen inhalation.

• #73 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  The role of bacterial airway colonisation in chronic stable asthma is unclear. However, there is increasing evidence for the role of bacterial pathogen-associated molecular patterns such as lipopolysaccharide in the activation of the innate immune system, which may lead to the expression of a neutrophilic asthma phenotype. […] Airway colonisation with potentially pathogenic bacteria is a common feature of severe asthma and is associated with a neutrophilic phenotype of airways inflammation. […] Mast cells play an important role in the pathogenesis of asthma. […] A defining feature of asthma is the presence of mast cells within the airway smooth muscle (ASM). […] These activated, histamine-depleted HLMC are still able to release equivalent amounts of histamine following IgE-dependent activation indicating that they can still respond to allergen inhalation.

• #74 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  The role of bacterial airway colonisation in chronic stable asthma is unclear. However, there is increasing evidence for the role of bacterial pathogen-associated molecular patterns such as lipopolysaccharide in the activation of the innate immune system, which may lead to the expression of a neutrophilic asthma phenotype. […] Airway colonisation with potentially pathogenic bacteria is a common feature of severe asthma and is associated with a neutrophilic phenotype of airways inflammation. […] Mast cells play an important role in the pathogenesis of asthma. […] A defining feature of asthma is the presence of mast cells within the airway smooth muscle (ASM). […] These activated, histamine-depleted HLMC are still able to release equivalent amounts of histamine following IgE-dependent activation indicating that they can still respond to allergen inhalation.

• #75 Understanding asthma pathogenesis | Thorax

  https://thorax.bmj.com/content/63/Suppl_7/A49

  Asthma is a major cause of morbidity and mortality worldwide. It is characterised by airway dysfunction and inflammation. A key determinant of the asthma phenotype is infiltration of airway smooth muscle bundles by activated mast cells. […] These findings suggest that mast cell localisation in the airway smooth muscle bundle promotes airway smooth muscle cell differentiation into a more contractile phenotype, thus contributing to the disordered airway physiology that characterises asthma.

• #76 Targeting cell signaling in allergic asthma | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-019-0079-0

  Asthma is chronic inflammation of the airways characterized by airway hyper-responsiveness, wheezing, cough, and dyspnea. The Th2 immune response is a major contributor to the pathophysiology of asthma. Targeted therapy modulating cell signaling pathways can be a powerful strategy to design new drugs to treat asthma. The potential molecular pathways that can be targeted include IL-4-IL-13-JAK-STAT-MAP kinases, adiponectin-iNOS-NF-B, PGD2-CRTH2, IFNs-RIG, Wnt/-catenin-FAM13A, FOXC1-miR-PI3K/AKT, JNK-Gal-7, Nrf2-ROS, Foxp3-RORt, CysLTR, AMP, Fas-FasL, PTHrP/PPAR, PAI-1, FcRI-LAT-SLP-76, Tim-3-Gal-9, TLRs-MyD88, PAR2, and Keap1/Nrf2/ARE. Therapeutic drugs can be designed to target one or more of these pathways to treat asthma. […] The disease usually presents with wheezing, cough, and dyspnea. Allergy and atopy comprise the main causes of asthma. Genetic and environmental triggers modulating the activation and regulation of the immune system (i.e., Th2 immune response) are the main orchestrators in the pathophysiology of asthma.

• #77 Targeting cell signaling in allergic asthma | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-019-0079-0

  Bronchial inflammation, smooth muscle spasm, and mucus production in allergic asthma are triggered by IL-4, IL-5, and IL-13, which are released by Th2 cells. IL-13 plays the main role in the excessive secretion of mucus and AHR. IL-5 participates in the activation and migration of eosinophils to airways triggering bronchial inflammation. IL-4 induces IgE isotype switching in B cells and upregulates high-affinity IgE receptor (FcRI) on the surface of target cells. […] The IL-4/IL-13/STAT-6 pathway is a key modulator of asthma pathophysiology. The activation of STAT-6 can be blocked by interfering with the interaction of STAT-6-MAP kinase with ERK1/2 and p38, as well as by suppressing STAT-6 serine phosphorylation, preventing STAT-6 acetylation, and inhibiting the recruitment of the p300 transcriptional coactivator.

• #78 Targeting cell signaling in allergic asthma | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-019-0079-0

  Several therapeutics have been introduced to interfere with the IL-4/IL-13/JAK/STAT-6 pathway. These include inhibitors of JAK, dimerization suppressors, phosphopeptides targeting the SH2 domain of STAT-6, decoy oligonucleotides, siRNAs, and finally synthetic small molecules. […] The Th2-high subtype is characterized by marked eosinophilic infiltration of the airways, whereas the Th2-low subtype is characterized by neutrophilic infiltration. […] The receptors of allergic cytokines, including IL-4, IL-5, IL-13, IL-31, and thymic stromal lymphopoietin (TSLP), trigger the JAK/STAT pathway. This is the main route involved in the pathogenesis of asthma. […] The activation of the Wnt signaling pathway was also shown to accelerate the proliferation of airway smooth muscle cells, which are involved in airway remodeling.

• #79 Mechanism behind obesity-related asthma identified | Harvard T.H. Chan School of Public Health

  https://hsph.harvard.edu/news/obesity-asthma-mechanism/

  Obesity-related asthma is poorly understood and very difficult to manage. In general, it is different from conventional allergic asthma and exercised-induced asthma, but certain clinical features are shared between them. One is airway hyperresponsiveness meaning that the airway narrows in response to a trigger, which causes difficulty breathing. […] Obesity is both a risk factor and a disease modifier for asthma, in that obesity increases the risk of developing asthma and asthma patients with obesity tend to have more symptoms and more exacerbations, and do not respond well to several standard asthma medications. […] We found that a hormone called cholecystokinin contributes in part to the airway narrowing that results in airflow limitation in obesity-related asthma. When we blocked the action of this hormone, we were able to improve airflow in the lungs of obese mice.

• #80 Mechanism behind obesity-related asthma identified | Harvard T.H. Chan School of Public Health

  https://hsph.harvard.edu/news/obesity-asthma-mechanism/

  Obesity-related asthma is poorly understood and very difficult to manage. In general, it is different from conventional allergic asthma and exercised-induced asthma, but certain clinical features are shared between them. One is airway hyperresponsiveness meaning that the airway narrows in response to a trigger, which causes difficulty breathing. […] Obesity is both a risk factor and a disease modifier for asthma, in that obesity increases the risk of developing asthma and asthma patients with obesity tend to have more symptoms and more exacerbations, and do not respond well to several standard asthma medications. […] We found that a hormone called cholecystokinin contributes in part to the airway narrowing that results in airflow limitation in obesity-related asthma. When we blocked the action of this hormone, we were able to improve airflow in the lungs of obese mice.

• #81 Mechanism behind obesity-related asthma identified | Harvard T.H. Chan School of Public Health

  https://hsph.harvard.edu/news/obesity-asthma-mechanism/

  We now provide evidence that cholecystokinin and CCKAR are involved in obesity-induced airway narrowing. The mechanism behind obesity-related asthma has been poorly understood, so this is a big step in the research. […] Yes, we found that existing pharmacological compounds that block CCKAR, known as CCKAR antagonists (proglumide, lorglumide, and devazepide), could lower asthma symptoms in obese mice. These compounds were originally intended to be used for other diseases such as stomach ulcers. They are generally safe to use without dangerous adverse effects. If our study is replicated in humans, we can then potentially use these compounds to treat asthma in people with obesity.

• #82 Asthma and Type 2 Diabetes: Link Between Conditions Not Explained by BMI Alone – Clinical Advisor

  https://www.clinicaladvisor.com/news/asthma-type-2-diabetes-link-not-explained-by-bmi-alone/

  We found an association between asthma and type 2 diabetes that was sustained after adjusting for BMI, indicating that BMI alone does not explain this relationship. […] We also found that the two conditions co-aggregate in siblings, indicating that the association is partly due to shared familial genetic and environmental risk factors.

• #83 Asthma and Type 2 Diabetes: Link Between Conditions Not Explained by BMI Alone – Clinical Advisor

  https://www.clinicaladvisor.com/news/asthma-type-2-diabetes-link-not-explained-by-bmi-alone/

  We found an association between asthma and type 2 diabetes that was sustained after adjusting for BMI, indicating that BMI alone does not explain this relationship. […] We also found that the two conditions co-aggregate in siblings, indicating that the association is partly due to shared familial genetic and environmental risk factors.

• #84 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #85 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #86 Asthma: Types, Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/6424-asthma

  Asthma causes bronchospasms, inflammation, thick mucus and constriction in the airways. […] The normal airways of a woman having an asthma attack become constricted, inflamed and full of mucus. […] Asthma has multiple causes: […] Allergies: Having allergies can raise your risk of developing asthma. […] Environmental factors: People can develop asthma after exposure to things that irritate the airways. These substances include allergens, toxins, fumes and second- or third-hand smoke. […] Genetics: If your family has a history of asthma or allergic diseases, you have a higher risk of developing the disease. […] Respiratory infections: Certain respiratory infections, such as respiratory syncytial virus (RSV), can damage young children’s developing lungs. […] Bronchodilators: These medicines relax the muscles around your airways. The relaxed muscles let the airways move air. They also let mucus move more easily through the airways. […] Anti-inflammatory medicines: These medicines reduce swelling and mucus production in your airways. They make it easier for air to enter and exit your lungs. […] Biologic therapies for asthma: These are used for severe asthma when symptoms persist despite proper inhaler therapy.

• #87 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #88 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #89 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #90 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #91 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #92 DUPIXENT® (dupilumab) Mechanism of Action For Asthma

  https://www.dupixenthcp.com/asthma/about/mechanism-of-action

  DUPIXENT is the only dual inhibitor of IL4 and IL13 signaling, two of the key drivers of local and systemic type 2 inflammation in asthma. […] The mechanism of dupilumab action has not been definitively established. […] IL-13 is a key source of local type 2 inflammation. When activated, it contributes to epithelial barrier dysfunction, eosinophilic inflammation, mucus overproduction and smooth muscle contraction. […] IL-4 is a key source of systemic type 2 inflammation that causes eosinophil trafficking to the site of inflammation. Eosinophils release eosinophilic cationic protein or ECP, eosinophil peroxidase or EPO, and other chemical mediators that contribute to asthma pathology. […] DUPIXENT binds to the IL-4 receptor blocking IL-4 and IL-13 intracellular signaling. […] DUPIXENT also binds to the IL-13 receptor preventing IL-13 receptor binding with IL-13 as well as complexing of IL-13 receptor with the IL-4 receptor complex. […] IL-4 and IL-13 contribute to multiple systemic inflammatory effects in asthma. […] IL-4 and IL-13 contribute to multiple local inflammatory effects in the bronchial tubes.

• #93 FAQs | FASENRA® (benralizumab) Subcutaneous Injection

  https://www.fasenra.com/faq

  FASENRA helps prevent asthma attacks (exacerbations) and may improve your breathing. Medicines such as FASENRA reduce blood eosinophils.* Eosinophils are a type of white blood cell that may contribute to your asthma. […] The mechanism of action of FASENRA in asthma is not fully understood. […] FASENRA is designed to target and remove eosinophils, a key cause of asthma. The mechanism of action of FASENRA in asthma is not fully understood.

• #94 FAQs | FASENRA® (benralizumab) Subcutaneous Injection

  https://www.fasenra.com/faq

  FASENRA helps prevent asthma attacks (exacerbations) and may improve your breathing. Medicines such as FASENRA reduce blood eosinophils.* Eosinophils are a type of white blood cell that may contribute to your asthma. […] The mechanism of action of FASENRA in asthma is not fully understood. […] FASENRA is designed to target and remove eosinophils, a key cause of asthma. The mechanism of action of FASENRA in asthma is not fully understood.

• #95 Montelukast (Singulair): Uses, Side Effects, Interactions, Pictures, Warnings & Dosing – WebMD

  https://www.webmd.com/drugs/2/drug-6478-8277/montelukast-oral/montelukast-oral/details

  Montelukast helps improve asthma symptoms by blocking substances in the body called leukotrienes that cause inflammation and swelling. […] Montelukast is commonly used for the long-term treatment of asthma and to prevent symptoms of exercise-induced asthma.

• #96 Montelukast (Singulair): Uses, Side Effects, Interactions, Pictures, Warnings & Dosing – WebMD

  https://www.webmd.com/drugs/2/drug-6478-8277/montelukast-oral/montelukast-oral/details

  Montelukast helps improve asthma symptoms by blocking substances in the body called leukotrienes that cause inflammation and swelling. […] Montelukast is commonly used for the long-term treatment of asthma and to prevent symptoms of exercise-induced asthma.

• #97 Montelukast: MedlinePlus Drug InformationLock

  https://medlineplus.gov/druginfo/meds/a600014.html

  Montelukast is used to prevent wheezing, difficulty breathing, chest tightness, and coughing caused by asthma in adults and children 12 months of age and older. […] Montelukast is in a class of medications called leukotriene receptor antagonists (LTRAs). It works by blocking the action of substances in the body that cause the symptoms of asthma and allergic rhinitis. […] Montelukast controls the symptoms of asthma and allergic rhinitis but does not cure these conditions. Continue to take montelukast even if you feel well. Do not stop taking montelukast without talking to your doctor.

• #98 What is the pathophysiology of asthma?

  https://www.medicalnewstoday.com/articles/asthma-pathophysiology

  The pathophysiology of asthma refers to the changes that occur in the airways and lungs that lead to asthma symptoms. Understanding the pathophysiology can help with targeting asthma treatment. […] The pathophysiology of asthma is the process or ways asthma alters the lungs. The exact process and impact on the lungs may differ slightly depending on the type of asthma someone has. However, the pathophysiology remains similar. Understanding the pathophysiology of asthma helps in determining effective treatment. […] Airflow obstruction, which occurs due to a reduction in the diameter of the airways, also develops as part of the asthma process. […] The airways become narrow due to the activation and release of immune cells, such as eosinophils, neutrophils, and mast cells. Inflammation develops as a response to the release of the cells, leading to the airways swelling.

• #99 What is the pathophysiology of asthma?

  https://www.medicalnewstoday.com/articles/asthma-pathophysiology

  The pathophysiology of asthma refers to the changes that occur in the airways and lungs that lead to asthma symptoms. Understanding the pathophysiology can help with targeting asthma treatment. […] The pathophysiology of asthma is the process or ways asthma alters the lungs. The exact process and impact on the lungs may differ slightly depending on the type of asthma someone has. However, the pathophysiology remains similar. Understanding the pathophysiology of asthma helps in determining effective treatment. […] Airflow obstruction, which occurs due to a reduction in the diameter of the airways, also develops as part of the asthma process. […] The airways become narrow due to the activation and release of immune cells, such as eosinophils, neutrophils, and mast cells. Inflammation develops as a response to the release of the cells, leading to the airways swelling.

• #100 What is the pathophysiology of asthma?

  https://www.medicalnewstoday.com/articles/asthma-pathophysiology

  The pathophysiology of asthma refers to the changes that occur in the airways and lungs that lead to asthma symptoms. Understanding the pathophysiology can help with targeting asthma treatment. […] The pathophysiology of asthma is the process or ways asthma alters the lungs. The exact process and impact on the lungs may differ slightly depending on the type of asthma someone has. However, the pathophysiology remains similar. Understanding the pathophysiology of asthma helps in determining effective treatment. […] Airflow obstruction, which occurs due to a reduction in the diameter of the airways, also develops as part of the asthma process. […] The airways become narrow due to the activation and release of immune cells, such as eosinophils, neutrophils, and mast cells. Inflammation develops as a response to the release of the cells, leading to the airways swelling.

• #101 What is the pathophysiology of asthma?

  https://www.medicalnewstoday.com/articles/asthma-pathophysiology

  The pathophysiology of asthma refers to the changes that occur in the airways and lungs that lead to asthma symptoms. Understanding the pathophysiology can help with targeting asthma treatment. […] The pathophysiology of asthma is the process or ways asthma alters the lungs. The exact process and impact on the lungs may differ slightly depending on the type of asthma someone has. However, the pathophysiology remains similar. Understanding the pathophysiology of asthma helps in determining effective treatment. […] Airflow obstruction, which occurs due to a reduction in the diameter of the airways, also develops as part of the asthma process. […] The airways become narrow due to the activation and release of immune cells, such as eosinophils, neutrophils, and mast cells. Inflammation develops as a response to the release of the cells, leading to the airways swelling.

• #102 What is the pathophysiology of asthma?

  https://www.medicalnewstoday.com/articles/asthma-pathophysiology

  Once this inflammatory response develops, it causes a cascade of adverse effects on the airways. For instance, it causes the airways smooth muscle to contract, leading to bronchoconstriction. The inflammation also causes excess mucus production in the airways, possibly forming a mucus plug. […] The pathophysiology of asthma is how the disease affects the normal function of the airways. It includes hypersensitivity of the airways, airflow obstruction, and reversibility. […] However, in some people, if asthma remains untreated and frequent attacks develop, the inflammation can cause structural changes in the airways. Developing airway remodeling, such as thickening and stiffening of the airway smooth muscle, can further cause airflow obstruction.

• #103 Severe Asthma vs Non-Severe Linked to Older Age, Female Sex, Higher BMI and BEC – Pulmonology Advisor

  https://www.pulmonologyadvisor.com/news/severe-vs-non-severe-asthma-adult-characteristics/

  Patients with severe asthma account for 4.6% of all asthma patients in Finland and are more likely to be female, older, and have higher body mass index (BMI) and blood eosinophils than patients with non-severe asthma. […] Severe asthma was defined in 11,081 individuals who met Global Initiative for Asthma (GINA) criteria for severe asthma for more than 1 year. […] The most significant predictors of the development of severe asthma included: being 51 to 60 years of age (odds ratio [OR], 3.90; 95% CI, 3.42-4.47), having chronic sinusitis (OR, 2.48; 95% CI, 2.12-2.89), and having a higher blood eosinophil count (600 cells/l; OR, 2.10; 95% CI, 1.56-2.28). […] The findings of this study identify the risk profile for the development of severe asthma and demonstrates that many of these factors are observed a year before the onset of severe asthma, the investigators concluded. […] Being 51 to 60 years old, having chronic sinusitis, and having BEC more than or equal to 600 cells/l conferred the highest risk of developing severe asthma in the following years.

• #104 Severe Asthma vs Non-Severe Linked to Older Age, Female Sex, Higher BMI and BEC – Pulmonology Advisor

  https://www.pulmonologyadvisor.com/news/severe-vs-non-severe-asthma-adult-characteristics/

  Patients with severe asthma account for 4.6% of all asthma patients in Finland and are more likely to be female, older, and have higher body mass index (BMI) and blood eosinophils than patients with non-severe asthma. […] Severe asthma was defined in 11,081 individuals who met Global Initiative for Asthma (GINA) criteria for severe asthma for more than 1 year. […] The most significant predictors of the development of severe asthma included: being 51 to 60 years of age (odds ratio [OR], 3.90; 95% CI, 3.42-4.47), having chronic sinusitis (OR, 2.48; 95% CI, 2.12-2.89), and having a higher blood eosinophil count (600 cells/l; OR, 2.10; 95% CI, 1.56-2.28). […] The findings of this study identify the risk profile for the development of severe asthma and demonstrates that many of these factors are observed a year before the onset of severe asthma, the investigators concluded. […] Being 51 to 60 years old, having chronic sinusitis, and having BEC more than or equal to 600 cells/l conferred the highest risk of developing severe asthma in the following years.

• #105 Severe Asthma vs Non-Severe Linked to Older Age, Female Sex, Higher BMI and BEC – Pulmonology Advisor

  https://www.pulmonologyadvisor.com/news/severe-vs-non-severe-asthma-adult-characteristics/

  Patients with severe asthma account for 4.6% of all asthma patients in Finland and are more likely to be female, older, and have higher body mass index (BMI) and blood eosinophils than patients with non-severe asthma. […] Severe asthma was defined in 11,081 individuals who met Global Initiative for Asthma (GINA) criteria for severe asthma for more than 1 year. […] The most significant predictors of the development of severe asthma included: being 51 to 60 years of age (odds ratio [OR], 3.90; 95% CI, 3.42-4.47), having chronic sinusitis (OR, 2.48; 95% CI, 2.12-2.89), and having a higher blood eosinophil count (600 cells/l; OR, 2.10; 95% CI, 1.56-2.28). […] The findings of this study identify the risk profile for the development of severe asthma and demonstrates that many of these factors are observed a year before the onset of severe asthma, the investigators concluded. […] Being 51 to 60 years old, having chronic sinusitis, and having BEC more than or equal to 600 cells/l conferred the highest risk of developing severe asthma in the following years.

• #106 Short-term exposure to fine particulate matter and asthma exacerbation: a large population-based case-crossover study in Southern Thailand | Environmental Health | Full Text

  https://ehjournal.biomedcentral.com/articles/10.1186/s12940-025-01182-7

  Asthma exacerbations remain a significant global health issue despite advances in management. Fine particulate matter (PM2.5, particles2.5 m in diameter) is a known trigger for asthma exacerbations. Chronic airway inflammation and bronchial remodeling are central to its pathogenesis. Common symptoms include cough, wheezing, shortness of breath, and chest tightness, which often occur at night and are triggered by factors such as air pollutants, particularly fine particulate matter (PM2.5, particles2.5 m in diameter), viral infections, and allergens. PM2.5 is a major environmental health risk, contributing substantially to the global burden of respiratory diseases, including asthma. Recent studies suggested that even low concentrations of PM2.5 can adversely affect health. Although previous studies demonstrated the acute effects of PM2.5 on asthma exacerbations and impaired lung function in high-pollution areas, research in regions with relatively low pollution, such as those affected by seasonal transboundary haze in Southeast Asia, remains limited. This study underscores the short-term effects of PM2.5 on asthma exacerbations, particularly during high-pollution episodes of transboundary haze in regions that generally experience low levels of air pollution. These findings emphasize the importance of achieving the WHO air quality targets to mitigate the health impacts from PM2.5. PM2.5 promotes the generation of reactive oxygen species in the airways, leading to allergic inflammation and airway hyperresponsiveness. However, the exact inflammatory pathways remain unclear.

• #107 Short-term exposure to fine particulate matter and asthma exacerbation: a large population-based case-crossover study in Southern Thailand | Environmental Health | Full Text

  https://ehjournal.biomedcentral.com/articles/10.1186/s12940-025-01182-7

  Asthma exacerbations remain a significant global health issue despite advances in management. Fine particulate matter (PM2.5, particles2.5 m in diameter) is a known trigger for asthma exacerbations. Chronic airway inflammation and bronchial remodeling are central to its pathogenesis. Common symptoms include cough, wheezing, shortness of breath, and chest tightness, which often occur at night and are triggered by factors such as air pollutants, particularly fine particulate matter (PM2.5, particles2.5 m in diameter), viral infections, and allergens. PM2.5 is a major environmental health risk, contributing substantially to the global burden of respiratory diseases, including asthma. Recent studies suggested that even low concentrations of PM2.5 can adversely affect health. Although previous studies demonstrated the acute effects of PM2.5 on asthma exacerbations and impaired lung function in high-pollution areas, research in regions with relatively low pollution, such as those affected by seasonal transboundary haze in Southeast Asia, remains limited. This study underscores the short-term effects of PM2.5 on asthma exacerbations, particularly during high-pollution episodes of transboundary haze in regions that generally experience low levels of air pollution. These findings emphasize the importance of achieving the WHO air quality targets to mitigate the health impacts from PM2.5. PM2.5 promotes the generation of reactive oxygen species in the airways, leading to allergic inflammation and airway hyperresponsiveness. However, the exact inflammatory pathways remain unclear.

• #108 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  Though asthma is a long-term disease, asthmatics can live a life without having asthma if they avoid their triggers and comply with their inhaled medications. […] Erhabor stated that the main thrust of asthma management is to use a combination therapy that acts as both a preventer and a reliever of asthma attacks and the progression of the disease. […] He said the symptoms of asthma are not what should be focused on but the underlying mechanism that causes asthma, which is the underlying inflammation. […] The underlying inflammation continues and may actually progress even when the patient is not having a visible attack, and that will lead to the airway becoming damaged. […] So in treating asthma, you look at this drug that will take care of the inflammation and the episodic attack.

• #109 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  Though asthma is a long-term disease, asthmatics can live a life without having asthma if they avoid their triggers and comply with their inhaled medications. […] Erhabor stated that the main thrust of asthma management is to use a combination therapy that acts as both a preventer and a reliever of asthma attacks and the progression of the disease. […] He said the symptoms of asthma are not what should be focused on but the underlying mechanism that causes asthma, which is the underlying inflammation. […] The underlying inflammation continues and may actually progress even when the patient is not having a visible attack, and that will lead to the airway becoming damaged. […] So in treating asthma, you look at this drug that will take care of the inflammation and the episodic attack.

• #110 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  Though asthma is a long-term disease, asthmatics can live a life without having asthma if they avoid their triggers and comply with their inhaled medications. […] Erhabor stated that the main thrust of asthma management is to use a combination therapy that acts as both a preventer and a reliever of asthma attacks and the progression of the disease. […] He said the symptoms of asthma are not what should be focused on but the underlying mechanism that causes asthma, which is the underlying inflammation. […] The underlying inflammation continues and may actually progress even when the patient is not having a visible attack, and that will lead to the airway becoming damaged. […] So in treating asthma, you look at this drug that will take care of the inflammation and the episodic attack.

• #111 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  Though asthma is a long-term disease, asthmatics can live a life without having asthma if they avoid their triggers and comply with their inhaled medications. […] Erhabor stated that the main thrust of asthma management is to use a combination therapy that acts as both a preventer and a reliever of asthma attacks and the progression of the disease. […] He said the symptoms of asthma are not what should be focused on but the underlying mechanism that causes asthma, which is the underlying inflammation. […] The underlying inflammation continues and may actually progress even when the patient is not having a visible attack, and that will lead to the airway becoming damaged. […] So in treating asthma, you look at this drug that will take care of the inflammation and the episodic attack.

• #112 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  According to her, some genes have been established to increase an individuals susceptibility to asthma, but it only plays out in the right environment and presence of its trigger. […] According to her, asthmas core symptoms, which are cough, chest tightness, wheeze and difficulty breathing, could be triggered by many factors, including smoke, dust, industrial pollution, pollens, cockroaches, and changes in weather. […] Dr Kehinde added that asthma sometimes occurs in association with other spectra of allergic diseases like allergic rhinitis, allergic conjunctivitis, atopic dermatitis, chronic obstructive lung diseases and gastro-oesophageal reflux disease.

• #113 Asthmatics can live without having asthma —Experts – Tribune Online

  https://tribuneonlineng.com/asthmatics-can-live-without-having-asthma-experts/

  According to her, some genes have been established to increase an individuals susceptibility to asthma, but it only plays out in the right environment and presence of its trigger. […] According to her, asthmas core symptoms, which are cough, chest tightness, wheeze and difficulty breathing, could be triggered by many factors, including smoke, dust, industrial pollution, pollens, cockroaches, and changes in weather. […] Dr Kehinde added that asthma sometimes occurs in association with other spectra of allergic diseases like allergic rhinitis, allergic conjunctivitis, atopic dermatitis, chronic obstructive lung diseases and gastro-oesophageal reflux disease.

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