Materiały źródłowe

• #1 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  Allergic rhinitis a chronic inflammatory disease of the upper airways that has a major impact on the quality of life of patients and is a socio-economic burden. Understanding the underlying immune mechanisms is central to developing better and more targeted therapies. The inflammatory response in the nasal mucosa includes an immediate IgE-mediated mast cell response as well as a late-phase response characterized by recruitment of eosinophils, basophils, and T cells expressing Th2 cytokines including interleukin (IL)-4, a switch factor for IgE synthesis, and IL-5, an eosinophil growth factor and on-going allergic inflammation. Recent advances have suggested new pathways like local synthesis of IgE, the IgE-IgE receptor mast cell cascade in on-going allergic inflammation and the epithelial expression of cytokines that regulate Th2 cytokine responses (i.e., thymic stromal lymphopoietin, IL-25, and IL-33).

• #1 Pathogenesis of allergic rhinitis (rhinosinusitis) – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-allergic-rhinitis-rhinosinusitis/print

  Pathogenesis of allergic rhinitis is presented in this topic review. […] Upon exposure to an allergen, atopic individuals respond by producing allergen-specific immunoglobulin E (sIgE). These IgE antibodies bind to IgE receptors on mast cells in the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the IgE antibodies are bridged on the cell surface by allergen, resulting in activation of the cell. Mast cells in the nasal tissues release preformed and granule-associated chemical mediators, which cause the symptoms of allergic rhinitis. […] Models of nasal allergen challenge in patients with allergic rhinitis have provided information about the pathogenesis of allergic rhinitis. […] The expression of allergic diseases of the upper airways reflects an autosomal dominant pattern of inheritance with incomplete penetrance. This inheritance pattern is manifested as a propensity to respond to inhalant allergen exposure by producing high levels of allergen-sIgE. The IgE response appears to be controlled by immune response genes located within the major histocompatibility complex (MHC) on chromosome 6.

• #1

  https://link.springer.com/article/10.1007/s12016-025-09028-3

  When an allergen enters the body for the first time, antigen-presenting cells transmit it to Th cells, which become activated and secrete cytokines such as IL-4 and IL-13. […] Those cytokines act on sIgGB cells to reconstitute and produce sIgE at the mucosal level. […] Localized sIgE in the mucous membranes plays a key role in the local allergic inflammatory response, and a variety of cytokines and immune cells interact with each other to influence IgE synthesis and allergic processes. […] Genomic studies have found a genetic association regarding AR pathogenesis. […] According to estimates, AR has a high hereditary component, with a heritability index of 0.65. […] Several reports have linked genetic loci and candidate genes to AR. […] Various causative genes of AR (e.g., SDAD1, CXCL10, and CXCL9) have been found to be related to an array of immune-related disorders.

• #1 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  Allergic rhinitis (AR) is the most common of all allergic disease affecting approximately 400 million people worldwide and is associated with a reduced quality of life of the patients, lower work productivity and school learning performance as well as increasing medical costs. Allergic rhinitis is an IgE-mediated inflammatory disease of the nasal mucous membranes due to the interaction of allergen characterized by an inflammatory infiltrate made up of eosinophils, T cells, mast cells and basophils, which release several mediators, chemokines and cytokines (among these, histamine and cysteinyl-leukotrienes are the major vasoactive mediators), regulation of the local and systemic IgE synthesis, and communication with the immune system and the bone marrow. […] The early or immediate phase response occurs in sensitized individuals within min of exposure to the allergen and lasts for about 2-3 h. One of the cardinal components of the early phase response is the degranulation of mast cells. In the sensitized individual mast cells are abundant in the epithelial compartment of the nasal mucosa and can be easily activated upon re-exposure to the allergens. Upon crosslinking of the allergen specific IgE bound to the surface of mast cells by the specific allergen, mast cells degranulate and release a variety of pre-formed and newly formed mediators leading to what is known as the early phase response. Histamine, which is the major mediator of allergic rhinitis, stimulates the sensory nerve endings of the Vth nerve (trigeminal) and induces sneezing. Histamine also stimulates the mucous glands causing the secretion of mucous (rhinorrhea) and histamine, leukotrienes and prostaglandins acts on the blood vessels causing nasal congestion.

• #1 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1

  Allergic rhinitis (AR) poses a global health problem and can be challenging to treat. […] The pathophysiology of AR is complex, comprising an early- and late-phase allergic response. The process is triggered by exposure to allergens such as pollen, mites, and/or animal dander that are recognised by antigen-specific immunoglobulin E (IgE) receptors on mast cells and basophils in presensitised individuals. The early-phase reaction is characterised by mast cell degranulation. This phase is associated with the rapid onset (over a period of minutes) of acute nasal symptoms (i.e. sneezing and rhinorrhoea) and the emergence of ocular symptoms (i.e. itching, redness, and watering). These symptoms are caused by histamine release, particularly from mast cells in the nasal mucosa. This early-phase histamine release, together with the effects of other potent pro-inflammatory cytokines (e.g. leukotrienes) and eicosanoids (e.g. prostaglandins and kinins) also increases vascular permeability, leading to oedema formation.

• #1 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  The late phase response is predominantly inflammatory in nature and is characterized by a inflammatory cellular influx comprising of predominantly T lymphocytes, basophils and eosinophils. A variety of mediators are released by these cells including leukotrienes, kinins, histamine which result in the continuation of the symptoms and the development of the late phase. The key to the orchestration of the late phase response lies in the production and release of a variety of cytokines and chemokines like IL-4, IL-13 from mast cells as these cytokines can upregulate the expression of 'adhesion molecules’ like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. […] Mast cells play a central role in the immune mechanisms of allergic rhinitis.

• #1 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/134825-overview

  The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction. […] Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days. […] Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.

• #1 Rhinitis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rhinitis_pathophysiology

  IgEallergen interaction result in the degranulation of mast cells and basophils with the release of preformed mediators such as histamine and tryptase, and the rapid de novo generation of other mediators, including cysteinyl leukotrienes (LTC4, LTD4, LTE4) and prostaglandins (primarily PGD2), producing the allergic response which result in itching, sneezing, rhinorrhoea and blockage in the nose. […] Mediators and cytokines released during the early response also act on postcapillary endothelial cells, promoting the expression of adhesion molecules(such as intercellular adhesion molecule 1, E-selectin, and vascular cell adhesion molecule 1). […] These adhesion molecules promote the adherence of circulating leukocytes, such as eosinophils, to endothelial cells. […] Factors with chemoattractant properties( such as IL-5 for eosinophils) also promote the infiltration of the superficial lamina propria of the mucosa with many eosinophils, some neutrophils and basophils, and eventually CD4+ (TH2) lymphocytes and macrophages. […] The role of IgE-mediated reaction in rhinitis and asthma have been further confirmed by the effect of an anti-IgE monoclonal antibody in these diseases.

• #1 Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells

  https://www.mdpi.com/2227-9059/10/10/2486

  Allergic rhinitis (AR) is a common rhinopathy that affects up to 30% of the adult population. It is defined as an inflammation of the nasal mucosa, develops in allergic individuals, and is detected mostly by a positive skin-prick test. AR is characterized by a triad of nasal congestion, rhinorrhea, and sneezing. […] IgE-dependent activation of MCs in the nasal mucosa following exposure to allergens in a sensitized individual is a cardinal mechanism in the pathophysiology of AR. […] As elaborated in detail later in this review, exposure to inhaled allergens in a sensitized individual starts the cascade leading to the AR symptoms via activation of MCs lining the nasal mucosa through crosslinking of antigens to a specific IgE antibody bound to the surface of MCs, resulting in the release of MC mediators.

• #1 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  In addition to the conventionally known mast cells mediators released when activated by an IgE-dependent mechanism in allergic rhinitis, mast cells release a variety of cytokines such as IL-4, IL-5, IL-6, IL-8, IL-10, IL-13 and TNF-. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. Eosinophils derive from the bone marrow from a progenitor cell (CD34+) that may develop into either eosinophils or basophils. Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. Th1 T cells release predominantly IFN- and IL-2 and are involved in the delayed hypersensitivity immune reactions, and Th2 T cells release predominantly IL-4 and IL-5 and are predominantly involved in IgE-mediated allergic inflammation.

• #1 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  The Regulatory T (Treg) cell is one of subsets of CD4+ cells, which suppresses the functions of other lymphocytes and are characterized by surface expression of CD4 and CD25 and nuclear expression of the transcription factor forkhead box P3 (FOXP3). […] The understanding that the mechanisms of disease generation provide a framework for rational therapy in this disorder, which will be based on the complex inflammatory reaction rather than on the symptoms alone is very important to the development of newer and more effective strategies of treatment.

• #1

  https://all-imm.com/index.php/aei/article/view/615

  Allergic rhinitis (AR) is a common otolaryngologic disease with frequent episodes of sneezing, clear nasal discharge flow and nasal congestion. The mechanisms of AR are complex and considered generally caused by the immune tolerance deficiency. Regulatory B cells (Bregs) are immunosuppressive cells that can modulate immune responses by the secretion of IL-10, IL-35, and tumor growth factor- (TGF-) and via the interaction of membrane surface molecules. However, Bregs are numerically deficient and/or dysfunctional in airway allergic diseases such as AR and allergic asthma, and the related mechanisms remain unclear. […] In this review, we summarize the role of Bregs in AR pathogenesis and highlight the importance of Bregs in maintaining immune tolerance. It is believed that further research on Bregs will contribute to developing new treatments and finding specific biomarkers that could help to predict disease progression.

• #1 Allergic rhinitis – Wikipedia

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

  Disruption of the nasal mucosal epithelial barrier may also release alarmins (a type of damage associated molecular pattern (DAMP) molecule) such as thymic stromal lymphopoietin, IL-25 and IL-33 which activate group 2 innate lymphoid cells (ILC2) which then also releases inflammatory cytokines leading to activation of immune cells.

• #1 Pathogenesis of rhinitis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/27434218/

  Rhinitis is a heterogeneous condition that has been associated with inflammatory responses as in allergic rhinitis but can also occur in the absence of inflammation such as in so-called idiopathic (previously 'vasomotor’) rhinitis. […] In allergic rhinitis, initial allergen exposure and sensitization involves antigen-presenting cells, T and B lymphocytes and results in the generation of allergen-specific T cells and allergen-specific IgE antibodies. […] On re-exposure to relevant allergens, cross-linking of IgE on mast cells results in the release of mediators of hypersensitivity such as histamine and immediate nasal symptoms. […] Within hours, there is an infiltration by inflammatory cells, particularly Th2 T lymphocytes, eosinophils and basophils into nasal mucosal tissue that results in the late-phase allergic response. […] Evidence for nasal priming and whether or not remodelling may be a feature of allergic rhinitis will be reviewed. […] The occurrence of so-called local allergic rhinitis in the absence of systemic IgE will be discussed.

• #1 The roles of toll like receptor 3, 7 and 8 in allergic rhinitis pathogenesis | Allergologia et Immunopathologia

  https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-avance-the-roles-toll-like-receptor-S0301054617301866

  Allergic rhinitis, as an allergic and nasal hypersensitivity disease, is associated with the inflammation of nasal mucosa. […] Toll-like receptors (TLRs) are the most important receptors of innate immunity; their crucial roles in the recognition of allergens and subsequently pathogenesis of allergic diseases have been evaluated recently. […] TLR3, 7 and 8 are the intracellular members of the innate immune receptors and recognize intracellular single and double strand RNAs. This review article collected the investigations regarding the roles of TLR3, 7 and 8 in the allergic rhinitis pathogenesis. […] Based on the crucial roles of innate immunity responses in human pro-inflammatory based diseases, it may be hypothesized that TLR3, 7 and 8 may play significant roles in the induction and progression of allergic rhinitis.

• #1 The roles of toll like receptor 3, 7 and 8 in allergic rhinitis pathogenesis | Allergologia et Immunopathologia

  https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-avance-the-roles-toll-like-receptor-S0301054617301866

  Increased expression of TLR3 on the mesenchymal stem cells in patients suffering from allergic rhinitis may propose that TLR3 may participate in the different functions of the cells during allergic rhinitis. […] In contrast to TLR3, it has been reported that TLR7 and TLR8, which recognize ssRNA rather than dsRNA, significantly participate in the amelioration of allergic rhinitis symptoms. […] Therefore, it appears that TLR7 and TLR8, as receptors for ssRNA, positively participate in the regulation of allergic rhinitis symptoms and can be considered as future targets for immunotherapy of allergic rhinitis. […] Based on the aforementioned data, increased expression of TLR3 and decreased expression of TLR7 and TLR8 may be considered as risk factors for the pathogenesis of allergic rhinitis. […] Therefore, it may be hypothesized that using antagonists of TLR3 and also agonists of TLR7 and TLR8 may be considered for future immunotherapy of allergic rhinitis.

• #1

  https://link.springer.com/article/10.1007/s12016-025-09028-3

  Proteomics focuses on the quantitative analysis, post-translational modifications, and interactions of protein molecules. […] To identify biomarkers relevant to the early diagnosis and treatment of AR, many researchers have performed proteomic analyses of specimens from different sources, such as serum, nasal lavage fluid (NLF), and nasal mucosa from AR patients. […] Metabolomics focuses on the discovery of new biomarkers and the monitoring of therapeutic effects. […] The production of key inflammatory mediators by the arachidonic acid (AA) metabolic network is considered to be a hallmark of various inflammation-related diseases. […] The microbiome is a functional entity that controls metabolism and regulates medication interactions. […] Increasing evidence suggests that patients with allergic diseases such as asthma, food allergy, atopic dermatitis, and AR have dysbiosis of the gut microbiota.

• #1 Research advances in the treatment of AR by probiotics | JAA

  https://www.dovepress.com/research-advances-in-the-treatment-of-allergic-rhinitis-by-probiotics-peer-reviewed-fulltext-article-JAA

  Probiotics can be used as immunomodulators and activators of the host defense pathway, in addition, oral probiotics can regulate the immune response of the respiratory system, and can prevent and treat upper respiratory diseases such as asthma, AR and other allergic diseases by modulating changes in the gut microbiota and immune response. […] Probiotics can activate Th1 or inhibit Th2, causing anti-inflammatory effects, and can also stimulate the production of immune factors such as interleukin 10 (IL-10), whose main role is to suppress inflammatory responses. […] Probiotics have the advantages of safety and high cost performance, therefore, the basic research and clinical application of probiotics for AR treatment are increasing. […] Probiotics can alleviate the inflammatory response of AR patients by improving the level of inflammatory factors in the serum, thereby alleviating their clinical symptoms.

• #1 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1

  The late-phase reaction develops over a period of hours after exposure to an allergen. It is characterised by cellular recruitment of basophils, neutrophils, T-lymphocytes, monocytes, and eosinophils, and by the release of multiple mediators, including cytokines, prostaglandins, and leukotrienes, which perpetuate the inflammatory response. This late-phase inflammatory reaction is associated with tissue remodelling, further tissue oedema, and the development and perpetuation of nasal congestion, considered by patients to be one of the most troublesome symptoms of AR. […] The pharmacological profiles of available treatments for AR show that there are a number of pathophysiological gaps within the AR pharmacopeia. For example, at concentrations achieved following clinical dosing, LTRAs are likely to be active predominantly at the leukotriene receptor, whereas OAHs at physiological concentrations will be active predominately at the H1 receptor.

• #1 Allergic Rhinitis (AR) Causes & Mechanisms | Haleon HealthPartner

  https://www.haleonhealthpartner.com/en-us/respiratory-health/conditions/allergic-rhinitis-conditions-home/allergic-rhinitis/allergic-rhinitis-causes-mechanism/

  The bodys immune response to allergens includes a series of early- and late-phase reactionsthe allergic cascade. There are several allergic mediators involved in this cascade, not just histamines. […] The end result is the allergic response consisting of a range of symptoms such as rhinorrhea (runny nose), sneezing, congestion, and pruritus (itching)2 […] INSs, often used as first-line treatment for patients with mild persistent or moderate-to-severe symptoms, work locally in the nasal mucosa to block multiple mediators involved in the allergic cascade, including histamine, cytokines, leukotrienes, chemokines, prostaglandins, and tryptase.

• #1 Treatment of Allergic Rhinitis | AAFP

  https://www.aafp.org/pubs/afp/issues/2015/1201/p985.html

  Many studies have demonstrated that intranasal corticosteroids are more effective than oral and intranasal antihistamines in the treatment of persistent or more severe allergic rhinitis. […] The leukotriene D4 receptor antagonist montelukast (Singulair) is comparable to oral antihistamines but is less effective than intranasal corticosteroids. […] Immunotherapy should be considered for moderate or severe persistent allergic rhinitis that is not responsive to usual treatments, in patients who cannot tolerate standard therapies or who want to avoid long-term medication use, and in patients with allergic asthma. […] Targeted immunotherapy, the only treatment that changes the natural course of allergic rhinitis, consists of administering a small amount of allergen extract subcutaneously or sublingually.

• #1 Mechanisms and Comparative Treatments of Allergic Rhinitis including Phototherapy

  https://www.mdpi.com/2313-5786/4/1/2

  Limitations in the conventional therapies mean that alternative treatments for AR are required. Intranasal phototherapy has received growing interest as an alternative treatment to relieve the symptoms of AR patients. AR is often treated using pharmacological products alone or in combination, depending on the symptoms suffered. Many affected by AR would like to reduce the requirement for medicines or may have other conditions where there are other side effects of the medicines. Many allergic rhinitis sufferers wish to reduce the amount of medication that they take. Many find that medication does not control their symptoms adequately. […] Phototherapy has therefore a role to play in the effective treatment of AR as it has effects on different inflammatory and immune-mediated mucosal symptoms. It is also shown to be effective where AR symptoms persist.

• #1 Research Progress on the New Mechanism of Acupuncture Treatment for Allergic Rhinitis

  https://www.heraldopenaccess.us/openaccess/research-progress-on-the-new-mechanism-of-acupuncture-treatment-for-allergic-rhinitis

  Acupuncture achieves the treatment of allergic rhinitis by modulating inflammatory mediators, modulating neuropeptide, acupuncture pterygopalatine ganglion during the same period, and bi-directionally modulating the sympathetic and parasympathetic nerves, etc. […] In the process of Allergic Rhinitis (AR), the release of inflammatory mediators such as histamine and leukotriene by Mast Cell (MC) and basophil granulocyte (Bas) degranulation is the direct cause of nasal mucosal dysfunction and clinical symptoms. […] Therefore, inhibiting the expression of inflammatory mediators such as histamine and leukotriene and regulating their levels in the serum is one of the commonly used means of treating AR at present. […] Studies have shown that acupuncture can effectively down-regulate the expression of H1R and H4R proteins in nasal mucosal tissues, inhibit the release of inflammatory mediator HA, attenuate or block the inflammatory reaction, and play a therapeutic role in the treatment of AR.

• #2 Overview on the pathomechanisms of allergic rhinitis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/

  Allergic rhinitis (AR) is the most common of all allergic disease affecting approximately 400 million people worldwide and is associated with a reduced quality of life of the patients, lower work productivity and school learning performance as well as increasing medical costs. Allergic rhinitis is an IgE-mediated inflammatory disease of the nasal mucous membranes due to the interaction of allergen characterized by an inflammatory infiltrate made up of eosinophils, T cells, mast cells and basophils, which release several mediators, chemokines and cytokines (among these, histamine and cysteinyl-leukotrienes are the major vasoactive mediators), regulation of the local and systemic IgE synthesis, and communication with the immune system and the bone marrow. […] The early or immediate phase response occurs in sensitized individuals within min of exposure to the allergen and lasts for about 2-3 h. One of the cardinal components of the early phase response is the degranulation of mast cells. In the sensitized individual mast cells are abundant in the epithelial compartment of the nasal mucosa and can be easily activated upon re-exposure to the allergens. Upon crosslinking of the allergen specific IgE bound to the surface of mast cells by the specific allergen, mast cells degranulate and release a variety of pre-formed and newly formed mediators leading to what is known as the early phase response. Histamine, which is the major mediator of allergic rhinitis, stimulates the sensory nerve endings of the Vth nerve (trigeminal) and induces sneezing. Histamine also stimulates the mucous glands causing the secretion of mucous (rhinorrhea) and histamine, leukotrienes and prostaglandins acts on the blood vessels causing nasal congestion.

• #2 Rhinitis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rhinitis_pathophysiology

  Allergic rhinitis is a multifactorial disease, its development is influenced by an interplay of genetic and environmental factors. […] Aeroallergens in the nasal tissue undergo antigen processing, eliciting allergen-specific allergic responses and also promoting the development of allergic airway disease. […] Allergic rhinitis is an IgE mediated disease. Genetic predisposition and environmental factors significantly influence its development. […] The inherent enzymatic proteolytic activity of aeroallergens promote their access to antigen presenting cells by cleaving tight junctions in the airway epithelium and also via activation of receptors on epithelial cells. […] These activated epithelial cells produce proinflammatory mediators (such as cytokines, chemokines, thymic stromal lymphopoietin) which interact with subepithelial and interepithelial dendritic cells.

• #2

  https://link.springer.com/article/10.1007/s12016-025-09028-3

  Those genes affect common genetic risk variants for atopic diseases, which implies that they can display typical pathogenic traits and be used for creating novel treatments. […] Epigenetic studies of AR have focused on several core aspects covering the regulation of gene expression, DNA methylation, histone modifications, and the role of non-coding RNAs. […] Research has demonstrated a correlation between the quantity and pattern of CD4+T cells in AR and the DNA methylation pattern, which can be used to differentiate allergic patients from healthy individuals. […] Transcriptomics creates an inevitable link between genomic genetic information and biological functions. […] The study of transcriptomics has helped scientists to understand how disease-causing genes in AR are regulated in different environments, at different developmental stages, and in disease states.

• #2 Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells

  https://www.mdpi.com/2227-9059/10/10/2486

  In addition to AR, MCs’ role is established in the pathogenesis of frequent comorbidities characterized by allergic inflammation such as atopic dermatitis (AD) and allergic asthma. […] The allergic reaction consists of an early phase mediated by the release of inflammatory mediators from preformed granules of MCs and a late phase characterized by the influx of inflammatory cells, which are mostly modulated by MCs and their secreted mediators. […] MCs promote the trafficking of immune cells to the site of infection or inflammation, making them an essential initiator of the inflammatory response. […] Through complex cellular processes, MCs can influence the induction, amplitude, and function of the adaptive immune response. […] In the nasal mucosa, APCs are located in paracellular and intercellular channels adjacent to the basal epithelial cells. APCs process inhaled allergen-derived proteins deposited in the nasal mucosa and present them to naïve CD4+ T lymphocytes (Th0s) in the draining lymph nodes.

• #2 Pathogenesis of allergic rhinitis (rhinosinusitis) – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-allergic-rhinitis-rhinosinusitis/print

  Pathogenesis of allergic rhinitis is presented in this topic review. […] Upon exposure to an allergen, atopic individuals respond by producing allergen-specific immunoglobulin E (sIgE). These IgE antibodies bind to IgE receptors on mast cells in the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the IgE antibodies are bridged on the cell surface by allergen, resulting in activation of the cell. Mast cells in the nasal tissues release preformed and granule-associated chemical mediators, which cause the symptoms of allergic rhinitis. […] Models of nasal allergen challenge in patients with allergic rhinitis have provided information about the pathogenesis of allergic rhinitis. […] The expression of allergic diseases of the upper airways reflects an autosomal dominant pattern of inheritance with incomplete penetrance. This inheritance pattern is manifested as a propensity to respond to inhalant allergen exposure by producing high levels of allergen-sIgE. The IgE response appears to be controlled by immune response genes located within the major histocompatibility complex (MHC) on chromosome 6.

• #2 Common allergens and immune responses of allergic rhinitis | JAA

  https://www.dovepress.com/common-allergens-and-immune-responses-associated-with-allergic-rhiniti-peer-reviewed-fulltext-article-JAA

  Allergen-specific IgE binds to high-affinity IgE Fc receptors on the surface of mast cells, or the allergen directly binds to the sensitized target cells IgE, thereby inducing the secretion of histamine, kininogenases, LTs, cytokines, and other mediators. […] The early allergen response can be attributed to the allergen-induced degranulation of nasal mast cells. […] The release of histamine from mast cells promotes H1 receptor activation. […] Mast cells are the primary effector cells in the early allergen response. Mast cells release cytokines and attract eosinophils, Th2 cells, and neutrophils to the nasal mucosa. […] The mediators released by mast cells, such as LTs, prostaglandins, and platelet-activating factors, lead to the observed reactions and immune chemotaxis, which further helps maintain inflammation.

• #2 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1

  The late-phase reaction develops over a period of hours after exposure to an allergen. It is characterised by cellular recruitment of basophils, neutrophils, T-lymphocytes, monocytes, and eosinophils, and by the release of multiple mediators, including cytokines, prostaglandins, and leukotrienes, which perpetuate the inflammatory response. This late-phase inflammatory reaction is associated with tissue remodelling, further tissue oedema, and the development and perpetuation of nasal congestion, considered by patients to be one of the most troublesome symptoms of AR. […] The pharmacological profiles of available treatments for AR show that there are a number of pathophysiological gaps within the AR pharmacopeia. For example, at concentrations achieved following clinical dosing, LTRAs are likely to be active predominantly at the leukotriene receptor, whereas OAHs at physiological concentrations will be active predominately at the H1 receptor.

• #2 Rhinitis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rhinitis_pathophysiology

  IgEallergen interaction result in the degranulation of mast cells and basophils with the release of preformed mediators such as histamine and tryptase, and the rapid de novo generation of other mediators, including cysteinyl leukotrienes (LTC4, LTD4, LTE4) and prostaglandins (primarily PGD2), producing the allergic response which result in itching, sneezing, rhinorrhoea and blockage in the nose. […] Mediators and cytokines released during the early response also act on postcapillary endothelial cells, promoting the expression of adhesion molecules(such as intercellular adhesion molecule 1, E-selectin, and vascular cell adhesion molecule 1). […] These adhesion molecules promote the adherence of circulating leukocytes, such as eosinophils, to endothelial cells. […] Factors with chemoattractant properties( such as IL-5 for eosinophils) also promote the infiltration of the superficial lamina propria of the mucosa with many eosinophils, some neutrophils and basophils, and eventually CD4+ (TH2) lymphocytes and macrophages. […] The role of IgE-mediated reaction in rhinitis and asthma have been further confirmed by the effect of an anti-IgE monoclonal antibody in these diseases.

• #2 Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells

  https://www.mdpi.com/2227-9059/10/10/2486

  As mentioned earlier, eosinophils engage MCs in a physical and soluble crosstalk via the AEU. […] TSLP, which is secreted by structural cells in the nasal mucosa, binds the TSLP receptor (TSLPR) expressed by MCs, inducing their release of various cytokines and chemokines (e.g., IL-5, IL-13, and CCL1). […] Research in the last two decades has provided increasing evidence that MCs critically contribute to innate host defense and adaptive immunity. MCs play an important role in the initiation and progression of several rhinopathies and the primary role in AR. MCs initiate the allergic inflammation cascade that leads to the development and maintenance of AR through the secretion of inflammatory mediators and interplay with different inflammatory cells in the nasal mucosa.

• #2 The Immunology of Asthma and Allergic Rhinitis | IntechOpen

  https://www.intechopen.com/chapters/67836

  In patients with allergic rhinitis, allergen-triggered early and late responses are mediated by a series of inflammatory cells. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Immunologic processes in both nasal and bronchial tissues involve TH2 lymphocytes and eosinophils. Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Eosinophils release an array of pro-inflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and might serve as a major source of IL-3, IL-5, GM-CSF, and IL-13. […] The respiratory tract is an important route of allergen entry. Several people react to airborne allergens with an IgE-mediated reaction, resulting from the deposition of mucosal mast cells beneath the nasal epithelium by allergens such as pollen that when they contact the epithelium, they release their soluble protein content, which is rich in eosinophils and allergic rhinitis characterized by intense itching, sneezing, nasal blockage, and irritation of the nasal mucosa due to histamine release.

• #2 Allergic rhinitis | Nature Reviews Disease Primers

  https://www.nature.com/articles/s41572-020-00227-0

  Palomares, O. et al. Mechanisms of immune regulation in allergic diseases: the role of regulatory T and B cells. Immunol. Rev. 278, 219-236 (2017). This is a comprehensive review discussing the role of regulatory T and B cells in the induction and maintenance of tolerance in allergic diseases, including AR. A deeper analysis of the molecular mechanism governing the generation of regulatory T cells and B cells in tolerance and discussion of how this could be exploited to develop alternative therapeutic interventions is also provided. […] Anto, J. M. et al. Mechanisms of the Development of Allergy (MeDALL): introducing novel concepts in allergy phenotypes. J. Allergy Clin. Immunol. 139, 388-399 (2017).

• #2

  https://all-imm.com/index.php/aei/article/view/615/944

  Allergic rhinitis (AR) is a common otolaryngologic disease with frequent episodes of sneezing, clear nasal discharge flow and nasal congestion. The mechanisms of AR are complex and considered generally caused by the immune tolerance deficiency. Regulatory B cells (Bregs) are immunosuppressive cells that can modulate immune responses by the secretion of IL-10, IL-35, and tumor growth factor- (TGF-) and via the interaction of membrane surface molecules. […] B lymphocytes are a major component of the immune system, and their effector functions are best known for producing antibodies, presenting antigens to T cells, and modulating immune responses through cytokine production. […] Recent studies have shown that the role of B cells in immune regulation cannot be ignored, especially in a subset of B cells, namely regulatory B cells (Bregs), which are characterized by secreting inhibitory cytokines (IL-10, IL-35, and TGF-) and can regulate the immune response in the body.

• #2 Allergic rhinitis – Wikipedia

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

  Disruption of the nasal mucosal epithelial barrier may also release alarmins (a type of damage associated molecular pattern (DAMP) molecule) such as thymic stromal lymphopoietin, IL-25 and IL-33 which activate group 2 innate lymphoid cells (ILC2) which then also releases inflammatory cytokines leading to activation of immune cells.

• #2 The Immunology of Asthma and Allergic Rhinitis | IntechOpen

  https://www.intechopen.com/chapters/67836

  Whereas allergic rhinitis results from activation of mucosal mast cells, asthma is triggered by allergen activation of submucosal mast cells in the lower airways. The nature and development airway inflammation may be driven by numerous factors, including pathogenic infections, pollution, or even relatively innocuous inhaled particles, such as allergens. […] Chronic allergen exposure leads to the continuous presence of increased number of lymphocytes, eosinophils, neutrophils, basophils, and other leukocytes causing airway hyper-reactivity and remodeling a thickening of the airway walls due to hyperplasia and hypertrophy of the smooth muscle layer, with the eventual development of fibrosis. […] In patients with allergic asthma endotypes, allergen can cause activation of mast cells in an antigen-specific manner. Also allergens can stimulate the airway epithelium, through toll-like receptors (TLRs) and other damage receptors, to release IL-25, IL33, and thymic stromal lymphopoietin (TSLP). These cytokines can lead to the activation of submucosal type two innate lymphoid cells (ILC2), inducing these to release IL-4, IL-5, IL-9, and IL-13.

• #2 Recent advances in the pathogenesis of rhinitis – Asthma Allergy Immunology

  https://aai.org.tr/abstract.php?lang=en&id=251

  Rhinitis is a term that describes the acute or chronic intermittent or persistent presence of more than one nasal symptoms including runny nose, itching, sneezing and stuffy nose. […] Although allergic rhinitis has a clear definition and its pathophysiology has been thoroughly investigated, nonallergic rhinitis remains poorly understood. […] In this review, we overview the conventional pathways in the pathophysiology of allergic, nonallergic rhinitis and then elaborate on the recent advances in the mechanisms. […] In addition, local allergic rhinitis; a new phenotype of rhinitis that may affect individuals previously diagnosed with nonallergic rhinitis is briefly highlighted.

• #2 Research advances in the treatment of AR by probiotics | JAA

  https://www.dovepress.com/research-advances-in-the-treatment-of-allergic-rhinitis-by-probiotics-peer-reviewed-fulltext-article-JAA

  Probiotics can be used as immunomodulators and activators of the host defense pathway, in addition, oral probiotics can regulate the immune response of the respiratory system, and can prevent and treat upper respiratory diseases such as asthma, AR and other allergic diseases by modulating changes in the gut microbiota and immune response. […] Probiotics can activate Th1 or inhibit Th2, causing anti-inflammatory effects, and can also stimulate the production of immune factors such as interleukin 10 (IL-10), whose main role is to suppress inflammatory responses. […] Probiotics have the advantages of safety and high cost performance, therefore, the basic research and clinical application of probiotics for AR treatment are increasing. […] Probiotics can alleviate the inflammatory response of AR patients by improving the level of inflammatory factors in the serum, thereby alleviating their clinical symptoms.

• #2 Treatment of Allergic Rhinitis | AAFP

  https://www.aafp.org/pubs/afp/issues/2015/1201/p985.html

  Allergic rhinitis is a common and chronic immunoglobulin E-mediated respiratory illness that can affect quality of life and productivity, as well as exacerbate other conditions such as asthma. […] Allergic rhinitis is an immunoglobulin E-mediated disease that occurs after exposure to indoor or outdoor allergens, such as dust mites, insects, animal dander, molds, and pollen. Symptoms include rhinorrhea, sneezing, and nasal congestion, obstruction, and pruritus. […] Optimal treatment includes allergen avoidance and pharmacotherapy. Targeted symptom control with immunotherapy and asthma evaluation should be considered when appropriate. […] Intranasal corticosteroids are the mainstay of treatment for allergic rhinitis. They act by decreasing the influx of inflammatory cells and inhibiting the release of cytokines, thereby reducing inflammation of the nasal mucosa.

• #2 Montelukast: MedlinePlus Drug InformationLock

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

  Montelukast is also used to treat the symptoms of seasonal (occurs only at certain times of the year), allergic rhinitis (a condition associated with sneezing and stuffy, runny or itchy nose) in adults and children 2 years of age and older, and perennial (occurs all year round) allergic rhinitis in adults and children 6 months of age and older. […] It works by blocking the action of substances in the body that cause the symptoms of asthma and allergic rhinitis.

• #2 Mechanisms and Comparative Treatments of Allergic Rhinitis including Phototherapy

  https://www.mdpi.com/2313-5786/4/1/2

  The effectiveness of phototherapy on allergic symptoms has been documented previously. The main trials where effects are reported are listed in Table 1. It is not possible to list all trials in summary as over 2000 trials/reports have been published on the beneficial effects of phototherapy. Many wavelengths of light used in phototherapy studies have been shown to be effective. These studies showed that phototherapy (UV-A, UV-B, visible light wavelengths and near-red and infra-red wavelengths) suppresses the clinical symptoms of allergic rhinitis. Most trials combined different wavelengths in treatments and this was shown to have a synergistic effect on the suppression of allergic rhinitis. […] The evidence shows that nostril-based application of phototherapy improves blood rheology and cerebral blood flow without needing to puncture blood vessels, indicating that this treatment may have equivalent results to peripheral intravenous laser irradiation. A potential problem of NIR light being in contact with skin is the heating effect. NIR light from an LED produces two types of energy, radiated NIR light energy which is absorbed by the skin and energy conducted as heat.

• #2 Research Progress on the New Mechanism of Acupuncture Treatment for Allergic Rhinitis

  https://www.heraldopenaccess.us/openaccess/research-progress-on-the-new-mechanism-of-acupuncture-treatment-for-allergic-rhinitis

  Studies have demonstrated that acupuncture can inhibit the expression of LTs by regulating the TLR4/NF-B signalling pathway, which can effectively reduce the content of LTs in the nasal cavity of AR rats, thereby reducing the inflammatory response and exerting a certain degree of alleviation of the symptoms associated with AR. […] Various neuropeptide are differentially expressed in the nasal mucosa of AR patients and animal models, and the acupuncture intervention can play a therapeutic role in the treatment of AR by regulating neuropeptides. […] Acupuncture can inhibit the expression of SP in the nasal mucosa by regulating the sensory nerve reflexes, thus alleviating nasal symptoms. […] Acupuncture can effectively regulate the balance of neuropeptides in the body, such as SP, VIP, and NPY, and regulate the balance of the body’s endocrine secretion, improve the symptoms of the patients, and improve the patients’ quality of life.

• #3 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1

  Allergic rhinitis (AR) poses a global health problem and can be challenging to treat. […] The pathophysiology of AR is complex, comprising an early- and late-phase allergic response. The process is triggered by exposure to allergens such as pollen, mites, and/or animal dander that are recognised by antigen-specific immunoglobulin E (IgE) receptors on mast cells and basophils in presensitised individuals. The early-phase reaction is characterised by mast cell degranulation. This phase is associated with the rapid onset (over a period of minutes) of acute nasal symptoms (i.e. sneezing and rhinorrhoea) and the emergence of ocular symptoms (i.e. itching, redness, and watering). These symptoms are caused by histamine release, particularly from mast cells in the nasal mucosa. This early-phase histamine release, together with the effects of other potent pro-inflammatory cytokines (e.g. leukotrienes) and eicosanoids (e.g. prostaglandins and kinins) also increases vascular permeability, leading to oedema formation.

• #3 Mechanisms and Comparative Treatments of Allergic Rhinitis including Phototherapy

  https://www.mdpi.com/2313-5786/4/1/2

  The late phase response occurs 4–6 h after antigen stimulation. The late phase has prolonged symptoms such as sneezing, rhinorrhea and nasal congestion which last for about 18–24 h. The late phase response is characterized by the inflammation of tissues and a cellular uptake of T lymphocytes, basophils and eosinophils. Other components released by these cells include leukotrienes, kinins and histamine, all of which result in the continuation of the symptoms. The activity of cytokines and chemokines like IL-4 and IL-13 that are secreted from mast cells is a key aspect of the late phase allergic response. […] The ARIA guidelines form an important part of decisions regarding the treatment of AR. These guidelines cover a range of treatment types. Self-management strategies are an important part of the ARIA guidelines. A system was proposed for a step-up or step-down of AR treatments from self-administration to emergency hospital admission. The guideline group aimed to adapt this approach to real-world evidence and the availability of medicines and resources.

• #3

  https://all-imm.com/index.php/aei/article/view/615/944

  Therefore, the present study aims to preliminarily explore the possible mechanism between Bregs and AR, and the prospects for the clinical application of Bregs in the treatment of AR. […] The regulation of allergen tolerance mediated by Bregs is regarded as an important immune tolerance mechanism of AR. […] The level of Bregs in AR patients is lower than that in healthy subjects and increased after immunotherapy. […] It is suggested that the recovery of nasal mucosal immunity and Bregs can be promoted by regulating the proportion and function of Tfh cells. […] Studies have shown that SIT of AR can enhance Bregs-mediated immune tolerance. The process includes increased Bregs level of specific IL-10 production, induction of Tregs l proliferation, significant increase of IgG-4 antibody level, inhibition of Th2 response, thus improving symptoms of AR and producing immune tolerance.

Zobacz więcej