Zapalenie oskrzeli
Patofizjologia i mechanizm

Zapalenie oskrzeli obejmuje ostre i przewlekłe postaci, różniące się etiologią i mechanizmami patogenetycznymi. Ostre zapalenie oskrzeli (OZO) jest najczęściej wirusowe (>90%), wywoływane przez rhinowirusy, enterowirusy, wirusy grypy A i B, paragrypy, koronawirusy (w tym SARS-CoV-2), metapneumowirus i RSV. Bakterie, głównie atypowe (Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis), stanowią 1-10% przypadków. Patogeneza OZO obejmuje zapalenie błony śluzowej oskrzeli, złuszczanie nabłonka, zwiększoną produkcję śluzu, upośledzenie klirensu śluzowo-rzęskowego oraz aktywację komórek zapalnych, co prowadzi do kaszlu, świszczącego oddechu i duszności. Przewlekłe zapalenie oskrzeli (PZO) definiuje się jako produktywny kaszel trwający ≥3 miesiące w roku przez ≥2 lata, najczęściej związane z paleniem tytoniu (90% pacjentów) i ekspozycją na zanieczyszczenia środowiskowe. W PZO obserwuje się hiperplazję komórek kubkowych, nadprodukcję śluzu, przewlekły naciek neutrofilowy i limfocytów T CD8+, przebudowę i włóknienie dróg oddechowych oraz oporność makrofagów na glikokortykosteroidy. Kluczową rolę odgrywa receptor EGFR, którego aktywacja indukuje ekspresję genów mucyny i hipersekrecję śluzu.

Zapalenie oskrzeli – patogeneza i mechanizm

Zapalenie oskrzeli to choroba charakteryzująca się stanem zapalnym dróg oddechowych, w szczególności oskrzeli, które są przewodami łączącymi tchawicę z płucami. Proces zapalny może dotyczyć zarówno ostrych, jak i przewlekłych postaci choroby, które różnią się mechanizmem patogenetycznym, czynnikami etiologicznymi oraz przebiegiem klinicznym.12

Patogeneza ostrego zapalenia oskrzeli

Ostre zapalenie oskrzeli (OZO) charakteryzuje się zapaleniem błony śluzowej oskrzeli, co najczęściej występuje jako następstwo infekcji górnych dróg oddechowych. Proces patogenetyczny rozpoczyna się od inokulacji nabłonka tchawiczo-oskrzelowego przez czynnik zakaźny, co prowadzi do stanu zapalnego, pogrubienia nabłonka oraz zwiększonej produkcji śluzu.34

W ponad 90% przypadków OZO ma etiologię wirusową. Najczęstszymi patogenami są:56

  • Rhinowirusy
  • Enterowirusy
  • Wirusy grypy A i B
  • Wirusy paragrypy
  • Koronawirusy (w tym SARS-CoV-2)
  • Ludzki metapneumowirus
  • Wirus oddechowy syncytialny (RSV)

Bakterie wykrywane są jedynie w 1-10% przypadków OZO. Wśród patogenów bakteryjnych wymienia się przede wszystkim bakterie atypowe, takie jak Mycoplasma pneumoniae, Chlamydophila pneumoniae oraz Bordetella pertussis.7

Mechanizm zapalenia obejmuje kilka kluczowych procesów:89

  • Zapalenie ściany oskrzeli prowadzące do pogrubienia błony śluzowej
  • Złuszczanie komórek nabłonka i obnażenie błony podstawnej
  • Zwiększony przepływ krwi i aktywacja komórkowa w zajętych oskrzelach
  • Upośledzenie funkcji układu rzęskowego oraz zmniejszenie klirensu śluzowo-rzęskowego
  • Nadmierna produkcja śluzu w odpowiedzi na podrażnienie

Stan zapalny w oskrzelach prowadzi do podrażnienia i ekspozycji zakończeń nerwów czuciowych, co wywołuje kaszel. Jednocześnie produkcja cytokin powoduje wyciek naczyniowy, zwiększoną sekrecję śluzu oraz rekrutację komórek zapalnych. Procesy te prowadzą do częściowej niedrożności dróg oddechowych, co może skutkować świszczącym oddechem i dusznością, podobnie jak w przypadku napadów astmy.1011

Patogeneza przewlekłego zapalenia oskrzeli

Przewlekłe zapalenie oskrzeli (PZO) definiuje się jako produktywny kaszel utrzymujący się przez co najmniej 3 miesiące w roku przez 2 kolejne lata, bez innych identyfikowalnych przyczyn. Jest to długotrwały stan zapalny dróg oddechowych, najczęściej związany z ekspozycją na dym tytoniowy lub inne zanieczyszczenia środowiskowe.1213

Kluczowe mechanizmy patogenetyczne w PZO obejmują:1415

  • Hiperplazja i hipertrofia komórek kubkowych i gruczołów śluzowych
  • Nadmierna produkcja i hipersekrecja śluzu
  • Upośledzenie klirensu śluzowo-rzęskowego
  • Przewlekły stan zapalny oskrzeli z naciekiem neutrofilów i limfocytów T CD8+
  • Przebudowa i włóknienie dróg oddechowych

W patogenezie przewlekłego zapalenia oskrzeli kluczową rolę odgrywa receptor naskórkowego czynnika wzrostu (EGFR), którego ekspresja i aktywacja są centralne dla hipersekrecji śluzu. Aktywacja EGFR wywołuje transkrypcję genów mucyny, co prowadzi do nadprodukcji i hipersekrecji śluzu. Proces ten jest dodatkowo nasilany przez neutrofile, które uwalniają elastazę neutrofilową.16

Ciągłe drażnienie dróg oddechowych powoduje:1718

  • Obrzęk i zapalenie dróg oddechowych
  • Przerost gruczołów śluzowych i zwiększenie liczby komórek kubkowych
  • Pogrubienie mięśni gładkich w drogach oddechowych, zwężające oskrzeliki
  • Produkcję nadmiernej ilości śluzu, który blokuje drogi oddechowe (odwracalna obturacja dróg oddechowych)
  • Postępujące zapalenie prowadzące do stopniowego niszczenia oskrzelików i włóknienia (nieodwracalna obturacja dróg oddechowych)

Mediatory zapalne i szlaki sygnałowe

W patogenezie zapalenia oskrzeli istotną rolę odgrywają liczne mediatory zapalne i szlaki sygnałowe:1920

  • Cytokiny prozapalne, takie jak TNF-α, IL-6, IL-1β – nasilają odpowiedź zapalną i stymulują produkcję śluzu
  • Interferon gamma (IFNG) – zaangażowany w odpowiedź immunologiczną na infekcje
  • Szlak JAK-STAT – reguluje ekspresję genów odpowiedzialnych za odpowiedź zapalną
  • Szlak TNF – kluczowy w mediowaniu zapalenia i uszkodzenia tkanek
  • Szlak PI3K-AKT – istotny w regulacji procesów zapalnych

W przewlekłym zapaleniu oskrzeli makrofagi odgrywają kluczową rolę w koordynowaniu odpowiedzi zapalnej. Badania wskazują, że makrofagi obecne w czopach śluzowych u pacjentów z przewlekłym zapaleniem oskrzeli są chronicznie aktywowane i wykazują oporność na glikokortykosteroidy. Utrzymują one stałą sekrecję sygnałów zapalnych zależnych od TNF, co napędza nadmierną produkcję śluzu przez komórki nabłonkowe.2122

Patomorfologia zapalenia oskrzeli

Zmiany patomorfologiczne w zapaleniu oskrzeli obejmują:2324

  • Pogrubienie ściany oskrzeli z obrzękiem błony śluzowej
  • Zwiększoną produkcję śluzu i zaleganie wydzieliny w świetle oskrzeli
  • Naciek komórek zapalnych (neutrofile, limfocyty T CD8+) w ścianie dróg oddechowych
  • Hiperplazję i hipertrofię gruczołów śluzowych – oceniana wskaźnikiem Reida (stosunek grubości warstwy gruczołów śluzowych do grubości ściany między nabłonkiem a chrząstką)
  • W przypadku przewlekłego zapalenia oskrzeli – włóknienie okołooskrzelowe i przebudowę małych dróg oddechowych

W oskrzelach osób cierpiących na przewlekłe zapalenie oskrzeli obserwuje się rozlane zapalenie z przewagą neutrofili oraz okołooskrzelową lokalizację zmian włóknistych. Jest to wynik działania interleukiny 8, czynników stymulujących kolonie i innych cytokin chemotaktycznych i prozapalnych. Komórki nabłonka dróg oddechowych uwalniają te mediatory zapalne w odpowiedzi na bodźce toksyczne, zakaźne i zapalne.25

Rola infekcji w zaostrzeniach zapalenia oskrzeli

Zaostrzenia przewlekłego zapalenia oskrzeli są często wywoływane przez infekcje bakteryjne, które mogą powodować zarówno bezpośrednie uszkodzenie toksyczne, jak i pośrednie uszkodzenie zapalne nabłonka oskrzelowego. Haemophilus influenzae jest głównym patogenem odpowiedzialnym za zaostrzenia, a powtarzające się epizody infekcji mogą być związane z szybszym pogorszeniem funkcji oddechowej.26

W przypadku ostrego zapalenia oskrzeli u dzieci, pierwotne infekcje, takie jak wirusowe zakażenia lub bakteryjne zapalenie płuc, mogą osłabić mechanizmy obronne płuc, prowadząc do nadmiernej produkcji śluzu, zmniejszonego klirensu śluzowo-rzęskowego i namnażania się bakterii, prawdopodobnie w postaci biofilmu.2728

Nieodpowiednio leczone przewlekłe bakteryjne zapalenie oskrzeli może prowadzić do przewlekłej choroby płuc z ropniami lub rozstrzeni oskrzeli. Zakłada się, że początkowa infekcja wirusowa zaburza funkcję nabłonka oddechowego i rzęsek, prowadząc do przewlekłego zapalenia sprzyjającego tworzeniu biofilmów bakteryjnych.29

Zapalenie oskrzeli a inne choroby układu oddechowego

Przewlekłe zapalenie oskrzeli jest jednym z kluczowych komponentów przewlekłej obturacyjnej choroby płuc (POChP). Mechanizmy patologiczne w POChP obejmują:303132

  • Zaburzenie równowagi między proteazami a antyproteazami, prowadzące do destrukcji tkanki płucnej
  • Aktywację neutrofili i makrofagów, skutkującą akumulacją wolnych rodników i uszkodzeniem antyproteaz
  • Chroniczny stan zapalny, który w zaawansowanej chorobie nie ustępuje mimo zaprzestania palenia
  • Stres mechaniczny na pęcherzyki płucne, zwiększający ich podatność na proteazy
  • Zwężenie i niedrożność dróg oddechowych spowodowane hipersekrecją śluzu, obrzękiem błony śluzowej, skurczem oskrzeli i włóknieniem okołooskrzelowym

Pacjenci z rozpoznaniem przewlekłego zapalenia oskrzeli, nawet bez cech obturacji, są narażeni na zwiększone ryzyko rozwoju POChP i wyższą śmiertelność z różnych przyczyn. Badania wykazały, że osoby poniżej 50 roku życia z przewlekłym zapaleniem oskrzeli i bez ograniczenia przepływu powietrza mają zwiększone ryzyko rozwoju POChP.33

Z kolei ostre zapalenie oskrzeli może prowadzić do zapalenia płuc u niektórych pacjentów, zwłaszcza tych z upośledzoną odpornością. Powtarzające się epizody ostrego zapalenia oskrzeli mogą również sugerować rozwój przewlekłej obturacyjnej choroby płuc.3435

Wpływ czynników środowiskowych i genetycznych

Najczęstszą przyczyną przewlekłego zapalenia oskrzeli jest palenie papierosów – około 90% pacjentów z przewlekłym zapaleniem oskrzeli to palacze. Inne czynniki środowiskowe obejmują:3637

  • Długotrwałą ekspozycję na zanieczyszczenia powietrza
  • Narażenie na pył i toksyczne gazy w środowisku lub miejscu pracy
  • Powtarzające się infekcje dróg oddechowych

Czynniki środowiskowe i genetyczne, w tym wpływy matczyne i z okresu dzieciństwa, odgrywają również kluczową rolę w rozwoju przewlekłego zapalenia oskrzeli. Interakcja między czynnikami genetycznymi a środowiskowymi determinuje podatność na rozwój choroby i jej przebieg.38

Leczenie zapalenia oskrzeli w kontekście patogenezy

Zrozumienie patogenezy zapalenia oskrzeli ma kluczowe znaczenie dla opracowania skutecznych strategii terapeutycznych:3940

  • W ostrym zapaleniu oskrzeli, które najczęściej ma etiologię wirusową, leczenie koncentruje się na edukacji pacjenta i opiece podtrzymującej.
  • Antybiotyki nie są zalecane w większości przypadków ostrego zapalenia oskrzeli, chyba że istnieją dowody na zakażenie bakteryjne (np. B. pertussis).
  • W przewlekłym zapaleniu oskrzeli leczenie może obejmować leki rozszerzające oskrzela, steroidy wziewne i mukolityki.

Badania nad nowymi metodami leczenia przewlekłego zapalenia oskrzeli obejmują interwencje celujące w podstawowe mechanizmy patogenetyczne. Przykładem jest system RejuvenAir, który wykorzystuje kriosprej do szybkiego zamrażania warstwy nabłonkowej ścian dróg oddechowych. Procedura ta niszczy uszkodzone rzęski i komórki kubkowe produkujące śluz, zachowując macierz pozakomórkową, co umożliwia regenerację zdrowych komórek.41

Badania nad tradycyjnymi preparatami roślinnymi również dostarczają obiecujących wyników. Przykładowo, Lianhuaqingwen (LHQW) wykazuje właściwości przeciwzapalne poprzez tłumienie odpowiedzi cytokinowej, co może pomóc w łagodzeniu przewlekłego zapalenia oskrzeli i zmniejszaniu uszkodzenia płuc. Mechanizm działania LHQW obejmuje inhibicję odpowiedzi zapalnych i szlaków sygnałowych, w szczególności poprzez oddziaływanie z kluczowymi celami molekularnymi (TNF, IL6, IFNG i STAT3).4243

Podsumowanie

Zapalenie oskrzeli to złożony proces patologiczny, którego mechanizmy różnią się w zależności od postaci ostrej lub przewlekłej. Ostre zapalenie oskrzeli najczęściej ma etiologię wirusową i charakteryzuje się przejściowym stanem zapalnym dróg oddechowych, podczas gdy przewlekłe zapalenie oskrzeli jest związane z długotrwałą ekspozycją na czynniki drażniące, prowadzącą do trwałych zmian strukturalnych w drogach oddechowych.4445

Zrozumienie złożonych mechanizmów patogenetycznych zapalenia oskrzeli umożliwia opracowanie skuteczniejszych strategii terapeutycznych ukierunkowanych na kluczowe procesy molekularne i komórkowe leżące u podstaw choroby. Przyszłe badania powinny koncentrować się na lepszym zrozumieniu interakcji między różnymi szlakami zapalnymi oraz na opracowaniu spersonalizowanych podejść terapeutycznych uwzględniających indywidualne czynniki genetyczne i środowiskowe.4647

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Acute Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK448067/
    Acute bronchitis is characterized by inflammation in the bronchi lining, is a frequent condition in emergency departments, urgent care centers, and primary care offices. […] The etiology of these symptoms arises from the inflammatory response within the lower respiratory tract, often triggered by viral infections. […] This condition primarily impacts the bronchial tree, leading to irritation, inflammation, and increased mucus production. Viral infections, such as the common cold or influenza viruses, adenovirus, and rhinovirus, are frequent instigators, although exposure to irritants or other respiratory pathogens can also be putative triggers. […] The inflammatory process triggers increased blood flow and cellular activity within the affected bronchi, resulting in heightened 18F-fluorodeoxyglucose (FDG) uptake when observed via positron-emission tomography (PET) scan.
  • #2 Bronchitis: Symptoms, causes, treatment, and more
    https://www.medicalnewstoday.com/articles/8888
    People with bronchitis have swelling and inflammation in their bronchial tubes, the air passages that link the mouth and nose with the lungs. […] Bronchitis is a condition that affects the bronchial tubes in the lungs. They may become inflamed, resulting in symptoms such as coughing and mucus production. […] It affects the body by narrowing the airways due to swelling, meaning less air can pass through. […] Chronic bronchitis results from repeated irritation and damage to the lung and airway tissues. The most common cause is smoking, but not everyone with bronchitis is a smoker. […] Other possible causes include long term exposure to air pollution, dust, and fumes from the environment. […] The symptoms of chronic bronchitis may resolve or improve for a while. However, they will come back or become worse again, especially if there is exposure to smoke or other triggers. […] Chronic bronchitis is an ongoing condition. If a person smokes and continues to smoke, they may develop worsening symptoms, emphysema, and COPD. All these conditions can be life threatening.
  • #3 Acute bronchitis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Acute_bronchitis_pathophysiology
    The pathologic process starts with the inoculation of tracheobranchial epithelium with invading organism, which leads to inflammation, thickening and increased mucus production. […] The causative agent is transmitted through the large and medium size airway tracts. […] Following transmission, the agent inoculates the tracheobronchial epithelium. […] This process leads to inflammation, thickening, and increased mucus production in the airways compared to normal bronchi as shown below:
  • #4 Bronchitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/297108-overview
    During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis. […] Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis. […] A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase.
  • #5 Acute Bronchitis | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/1001/p560.html
    Acute bronchitis is most often caused by a viral infection. The most commonly identified viruses are rhinovirus, enterovirus, influenza A and B, parainfluenza, coronavirus, human metapneumovirus, and respiratory syncytial virus. Bacteria are detected in 1% to 10% of cases of acute bronchitis. Atypical bacteria, such as Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Bordetella pertussis, are rare causes of acute bronchitis. […] Approximately 10% of patients presenting with a cough lasting at least two weeks have evidence of B. pertussis infection. During outbreaks, pertussis detection is more likely in children and those with prolonged coughs. Antibiotics can eradicate B. pertussis from the nasopharynx. They do not seem to shorten the course of illness unless given in the first one to two weeks.
  • #6 Acute Bronchitis – Lung and Airway Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/lung-and-airway-disorders/acute-bronchitis/acute-bronchitis
    Acute bronchitis is inflammation of the windpipe (trachea) and the airways that branch off the trachea (bronchi) caused by infection. […] Acute bronchitis is usually caused by a viral upper respiratory tract infection. […] Acute bronchitis is caused by infection due to: Viruses (most common), Bacteria. […] Viral bronchitis may be caused by a number of common viruses, including the influenza virus and the viruses that cause the common cold, including respiratory syncytial virus (RSV). Acute bronchitis can also occur as part of the SARS-CoV-2 infection. […] Bacteria cause less than one in 20 cases of bronchitis. Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis infection (which causes whooping cough) are among the bacteria that cause acute bronchitis. […] Sometimes excessive levels of air pollution or breathing in toxic fumes can also inflame the airways and cause bronchitis.
  • #7 Acute Bronchitis | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/1001/p560.html
    Acute bronchitis is most often caused by a viral infection. The most commonly identified viruses are rhinovirus, enterovirus, influenza A and B, parainfluenza, coronavirus, human metapneumovirus, and respiratory syncytial virus. Bacteria are detected in 1% to 10% of cases of acute bronchitis. Atypical bacteria, such as Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Bordetella pertussis, are rare causes of acute bronchitis. […] Approximately 10% of patients presenting with a cough lasting at least two weeks have evidence of B. pertussis infection. During outbreaks, pertussis detection is more likely in children and those with prolonged coughs. Antibiotics can eradicate B. pertussis from the nasopharynx. They do not seem to shorten the course of illness unless given in the first one to two weeks.
  • #8 Acute Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK448067/
    The inflammation of the bronchial wall leads to mucosal thickening, epithelial cell desquamation, and denudation of the basement membrane. In some instances, a viral upper respiratory infection can progress to a lower respiratory tract infection, resulting in acute bronchitis. […] Acute bronchitis is inflammation affecting the large and mid-sized airways (bronchi), frequently precipitated by viral infections. […] The majority (90%) of cases are caused by viruses, resulting in inflammation and increased mucus production.
  • #9 Bronchitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/297108-overview
    During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis. […] Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis. […] A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase.
  • #10 Acute Bronchitis in Childhood | IntechOpen
    https://www.intechopen.com/chapters/87314
    There will be a discussion of the manifestation of acute bronchitis in children and note differences with that seen in the adult population. […] Understanding the differing pathophysiology of afferent hypersensitivity and inflammatory infiltrates in the bronchial epithelium enables for different therapeutic approaches. […] The inflammatory response in the lung protects the person from microorganisms or particles which may reach the airway surface. It augments other host defense mechanisms such as mucociliary clearance, defensins, and immunoglobulins. If the response is inadequate to eradicate offending substances, the subsequent inflammatory process can damage lung tissue in addition to any direct toxic or deleterious effects by the infectious organisms or particles. […] The cough results from viral infection of epithelial cells and shedding of necrotic cells into the airway exposing sensory nerve endings. Attempts to control the infection involve the production of cytokines causing vascular leak, mucus secretion, and recruitment of inflammatory cells. These result in some blockage of the airway which may further invoke coughing to remove the mixture of secretions and mucus. Coughing resolves with control of the viral infection.
  • #11 Acute Bronchitis – Lung and Airway Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/lung-and-airway-disorders/acute-bronchitis/acute-bronchitis
    Because bronchitis can temporarily narrow the airways, people may develop wheezing and/or shortness of breath, as well as chest tightness due to the narrowing, and/or chest pain due to incessant coughing, similar to what happens in an asthma attack. […] A viral bronchitis can lead to infection of the lung tissue (pneumonia) either by itself or by a secondary bacterial infection. […] Doctors usually make a diagnosis of acute bronchitis based on the symptoms. […] Doctors rarely do tests to find the cause of acute bronchitis, and blood tests are not helpful. […] Antibiotics do not help viral bronchitis. Since most acute bronchitis is viral, doctors give antibiotics only when the infection is clearly caused by bacteria (for example, during an outbreak) or when the symptoms are getting worse over time rather than improving, indicating a secondary bacterial infection. […] Acute bronchitis is usually treated best without using an antibiotic.
  • #12 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Chronic bronchitis is a long-term inflammatory condition of the airways, characterized by a persistent productive cough without other identifiable underlying causes lasting at least 3 months per year for 2 consecutive years. […] Chronic bronchitis leads to excessive mucus production, causing airway obstruction and inflammation. […] Goblet cell hyperplasia leads to excessive mucus production. This, combined with reduced mucus clearance, causes airway inflammation, structural changes, and obstruction. […] In adults with chronic bronchitis, cigarette smoke exposure, recurrent or chronic viral and bacterial infections, or toxic environmental exposures stimulate mucus overproduction and hypersecretion, and inflammatory and humoral mediators stimulate the release of mucin to protect the airway against noxious stimuli.
  • #13 Bronchitis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bronchitis/symptoms-causes/syc-20355566
    Bronchitis is an inflammation of the lining of your bronchial tubes. These tubes carry air to and from your lungs. […] Chronic bronchitis, a more serious condition, is a constant irritation or inflammation of the lining of the bronchial tubes, often due to smoking. […] The most common cause of chronic bronchitis is cigarette smoking. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition. […] Although a single episode of bronchitis usually isn’t cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis, however, may mean that you have chronic obstructive pulmonary disease (COPD).
  • #14 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Chronic bronchitis is a long-term inflammatory condition of the airways, characterized by a persistent productive cough without other identifiable underlying causes lasting at least 3 months per year for 2 consecutive years. […] Chronic bronchitis leads to excessive mucus production, causing airway obstruction and inflammation. […] Goblet cell hyperplasia leads to excessive mucus production. This, combined with reduced mucus clearance, causes airway inflammation, structural changes, and obstruction. […] In adults with chronic bronchitis, cigarette smoke exposure, recurrent or chronic viral and bacterial infections, or toxic environmental exposures stimulate mucus overproduction and hypersecretion, and inflammatory and humoral mediators stimulate the release of mucin to protect the airway against noxious stimuli.
  • #15 Chronic Bronchitis: Pathophysiology | RESPe
    https://www.respelearning.scot/topic-2-assessment-and-common-lung-diseases/common-lung-diseases/copd/chronic-bronchitis
    In chronic bronchitis exposure to an irritant over many years causes inflammation in the lungs which leads to the following changes: […] Continual irritants (smoking, infection, pollution) to the lungs cause the airways to become swollen and inflamed. […] Constant irritants lead to hypertrophy (enlargement) of the mucus-secreting glands of the bronchial tree, an increase in the number of goblet cells, which results in increased mucus secretion. […] The smooth muscle in the airways becomes thicker and narrows the bronchioles. […] Extra mucus is produced to trap any irritants and prevent them entering the lungs. […] The cilia become unable to cope with excessive secretions and therefore the mucus blocks the airways. This is known as Reversible Airways Obstruction. […] The mucus goes deeper into the lungs and becomes harder to clear.
  • #16 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    In addition, inflammatory cells activate the epidermal growth factor receptor (EGFR), which triggers mucin gene transcription. This process leads to the overproduction and hypersecretion of mucus by the increased activation and degranulation of neutrophils due to neutrophil-mediated elastase. […] EGFR receptor expression and activation are central to mucus hypersecretion, with activated neutrophil involvement being key. […] Experts believe high mucin concentration is the primary culprit of faulty mucus transport and intrapulmonary mucus accumulation. […] Mucous metaplasia obstructs airflow due to mucus hypersecretion and thickening of the epithelial cell layer. […] Inadequate clearing of mucus leads to infection and inflammation of the airways. […] The presence of chronic cough and sputum production increases the risk of developing COPD regardless of smoking status.
  • #17 Chronic Bronchitis: Pathophysiology | RESPe
    https://www.respelearning.scot/topic-2-assessment-and-common-lung-diseases/common-lung-diseases/copd/chronic-bronchitis
    In chronic bronchitis exposure to an irritant over many years causes inflammation in the lungs which leads to the following changes: […] Continual irritants (smoking, infection, pollution) to the lungs cause the airways to become swollen and inflamed. […] Constant irritants lead to hypertrophy (enlargement) of the mucus-secreting glands of the bronchial tree, an increase in the number of goblet cells, which results in increased mucus secretion. […] The smooth muscle in the airways becomes thicker and narrows the bronchioles. […] Extra mucus is produced to trap any irritants and prevent them entering the lungs. […] The cilia become unable to cope with excessive secretions and therefore the mucus blocks the airways. This is known as Reversible Airways Obstruction. […] The mucus goes deeper into the lungs and becomes harder to clear.
  • #18 Chronic Bronchitis: Pathophysiology | RESPe
    https://www.respelearning.scot/topic-2-assessment-and-common-lung-diseases/common-lung-diseases/copd/chronic-bronchitis
    Excessive secretions are liable to infection. […] The walls of the bronchioles become inflamed, continual inflammation causes gradual destruction of the bronchioles, resulting in fibrosis – Irreversible Airways Obstruction. […] Disease progression can also affect the pulmonary blood vessels […] If the inflammation spreads to the blood vessels this will lead to capillary bed wall atrophy (wasting). This increases the pressure of the pulmonary circulation. Pulmonary arteries may become distended (stretched) and blood may back track into the right side of the heart resulting in right sided hypertrophy (enlargement) and heart failure. This is known as Cor Pulmonale.
  • #19 Lung macrophages drive mucus production and steroid-resistant inflammation in chronic bronchitis | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01762-4
    Patients with chronic obstructive pulmonary disease (COPD) frequently suffer from chronic bronchitis (CB) and display steroid-resistant inflammation with increased sputum neutrophils and macrophages. […] We demonstrate that sputum plug macrophages isolated from COPD patients with chronic bronchitis (COPD/CB) are chronically activated and only partially respond to ex vivo corticosteroid treatment compared to alveolar macrophages isolated from lung resections. […] Our data pinpoint a critical role for chronically activated sputum macrophages in perpetuating TNF-dependent signals driving mucus hyper-production. […] In COPD/CB, macrophages are believed to play a major role in orchestrating the inflammatory response. […] Even though the clinical manifestations of CB are well characterized, little is known about the underlying signaling driving sputum hyper-production and the contribution of different cell types to the clinically observed corticosteroid resistance in this chronic inflammatory disease.
  • #20 Exploring the mechanism of Lianhuaqingwen (LHQW) in treating chronic bronchitis based on network pharmacology and experimental validation | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-02927-7
    Lianhuaqingwen (LHQW) has been used in the treatment of chronic bronchitis, but the precise mechanism through which LHQW exhibits its anti-inflammatory effects in this context is not yet fully understood. […] The development of chronic bronchitis is a multifaceted process influenced by the intricate regulation of numerous genes and proteins. […] LHQW possesses anti-inflammatory properties by suppressing cytokine responses, which may help in addressing chronic bronchial inflammation and reducing lung injury. […] By constructing a protein-protein interaction (PPI) network for the 76 potential gene targets, four core targets (TNF, IL6, IFNG, and STAT3) were identified as primarily involved in responses to lipopolysaccharide, the TNF pathway, and the JAK-STAT pathway. […] Molecular docking results revealed a favorable affinity between multiple active ingredients of LHQW and the four core targets, suggesting that the therapeutic effects are mediated through the inhibition of inflammatory responses and signaling pathways.
  • #21 Lung macrophages drive mucus production and steroid-resistant inflammation in chronic bronchitis | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01762-4
    Patients with chronic obstructive pulmonary disease (COPD) frequently suffer from chronic bronchitis (CB) and display steroid-resistant inflammation with increased sputum neutrophils and macrophages. […] We demonstrate that sputum plug macrophages isolated from COPD patients with chronic bronchitis (COPD/CB) are chronically activated and only partially respond to ex vivo corticosteroid treatment compared to alveolar macrophages isolated from lung resections. […] Our data pinpoint a critical role for chronically activated sputum macrophages in perpetuating TNF-dependent signals driving mucus hyper-production. […] In COPD/CB, macrophages are believed to play a major role in orchestrating the inflammatory response. […] Even though the clinical manifestations of CB are well characterized, little is known about the underlying signaling driving sputum hyper-production and the contribution of different cell types to the clinically observed corticosteroid resistance in this chronic inflammatory disease.
  • #22 Lung macrophages drive mucus production and steroid-resistant inflammation in chronic bronchitis | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01762-4
    We hypothesized that the highly neutrophilic and pro-inflammatory cytokine milieu in sputum plugs may drive development of a steroid-resistant, chronically activated macrophage phenotype that constantly secretes inflammatory signals driving mucus hyper-production by epithelial cells. […] Given the importance of TNF as mediator in the mechanistic macrophage-epithelial cross-talk assay and the chronic TNF expression observed in the clinically sampled sputum macrophages, the effect of the corticosteroid dexamethasone was investigated by measuring the amount of TNF protein released into the media of ex vivo cultured sputum and alveolar macrophages. […] Taken together, these data show that, in contrast to alveolar macrophages from either COPD or non-COPD donors, sputum macrophages from COPD chronic bronchitis patients are steroid resistant. […] In conclusion, our data pinpoint a critical role for sputum macrophages in chronic bronchitis by perpetuating macrophage-epithelial signaling that can drive aberrant mucin expression in bronchial epithelial cells.
  • #23 Bronchitis pathophysiology – wikidoc
    https://wikidoc.org/index.php/Bronchitis_pathophysiology
    Bronchitis is the inflammatory response of the bronchial epithelium to infections or irritants. The pathophysiological findings seen with acute bronchitis include: wall thickening, inflammation, and increased mucus production. When the process becomes chronic, bronchial mucociliary function decreases, leading to airway clogging by debris and copious mucus secretion. […] Inflammatory response of the bronchial epithelium to infectious agents or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa. […] Hallmark features include: hyperplasia and hypertrophy of the goblet cells of the airway, resulting in an increase in secretion of mucus, which contributes to airway obstruction. […] On microscopic histopathological analysis, chronic bronchitis shows infiltration of the airway walls with inflammatory cells, particularly CD8+ T-lymphocytes and neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airways. Further progression leads to metaplasia and fibrosis of the lower airway. The consequence of these changes is a limitation of airflow.
  • #24 COPD (Emphysema and Chronic Bronchitis): From Diagnosis to Treatment – Manual of Medicine
    https://manualofmedicine.com/topics/pulmonology/copd-emphysema-chronic-bronchitis-diagnosis-treatment/
    The hallmark of chronic bronchitis is hypertrophy of the mucus-producing glands found in the submucosa of large cartilaginous airways. Quantitation of this anatomic change is based on the ratio of the thickness of the submucosal glands to that of the bronchial wall. […] In lungs from patients with COPD studied at post-mortem there is goblet cell hyperplasia, mucosal and submucosal inflammatory cells, edema, peribronchial fibrosis, intraluminal mucus plugs, and increased smooth muscle in small airways. […] Inflammation in chronic bronchitis occurs at the alveolar epithelium and differs from the predominantly eosinophilic inflammation of asthma by the predominance of neutrophils and the peribronchiolar location of fibrotic changes. […] Emphysema is classified according to the pattern of involvement of the gas-exchanging units (acini) of the lung distal to the terminal bronchiole.
  • #25 Bronchitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/297108-overview
    During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis. […] Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis. […] A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase.
  • #26
    https://journals.lww.com/co-pulmonarymedicine/abstract/1996/05000/infective_pathogenesis_and_outcomes_in_chronic.4.aspx
    Bacterial infection is an important cause of exacerbations of chronic bronchitis, which can precipitate both direct toxic and host-mediated inflammatory bronchial epithelial damage. […] Repeated episodes, especially when caused by Haemophilus influenzae (the major pathogen) may be associated with more rapid deterioration in respiratory function. […] Antibiotic therapy has an accepted place in management, and predictors of the outcome of exacerbations have now been developed that allow severity staging of individual episodes. […] Nevertheless, despite the recognition of excessive failure rates due to increasing bacterial resistance and poor respiratory kinetics, many patients continue to receive empiric therapy with amoxicillin and other oral -lactams. […] This will enable both an assessment of their place in the management of exacerbations in at-risk patients with severe disease and an evaluation of their longer-term role in the prevention of a decline in respiratory function consequent upon repeated and ineffectively treated exacerbations.
  • #27 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Studies reveal that patients younger than 50 with chronic bronchitis and no airflow limitation are at increased risk of developing COPD and all-cause mortality. […] In children, initial insults, like viral infections or bacterial pneumonia, weaken the lung’s defenses, leading to excessive mucus production, reduced mucociliary clearance, and bacterial overgrowth, most likely in a biofilm. […] Environmental and genetic factors, including maternal and childhood influences, also play a key role.
  • #28 Pediatric Bronchitis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1001332-overview
    The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and an airway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study data have identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airway disease. ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease, including mucous obstruction, goblet cell hyperplasia, and chronic inflammatory cell infiltration. […] A chronic or recurrent insult to the airway epithelium, such as recurrent aspiration or repeated viral infection, may contribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection with commonly isolated airway organisms may occur. The most common bacterial pathogen that causes lower respiratory tract infections in children of all age groups is Streptococcus pneumoniae. […] It is speculated that an initial viral infection disrupts respiratory epithelial and ciliary function, leading to chronic inflammation supporting the formation of bacterial biofilms. If untreated, protracted bacterial bronchitis may lead to chronic suppurative lung disease or bronchiectasis.
  • #29 Pediatric Bronchitis: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1001332-overview
    The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and an airway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study data have identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airway disease. ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease, including mucous obstruction, goblet cell hyperplasia, and chronic inflammatory cell infiltration. […] A chronic or recurrent insult to the airway epithelium, such as recurrent aspiration or repeated viral infection, may contribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection with commonly isolated airway organisms may occur. The most common bacterial pathogen that causes lower respiratory tract infections in children of all age groups is Streptococcus pneumoniae. […] It is speculated that an initial viral infection disrupts respiratory epithelial and ciliary function, leading to chronic inflammation supporting the formation of bacterial biofilms. If untreated, protracted bacterial bronchitis may lead to chronic suppurative lung disease or bronchiectasis.
  • #30 Chronic Obstructive Pulmonary Disease (COPD) – Pulmonary Disorders – MSD Manual Professional Edition
    https://www.msdmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd
    Chronic obstructive bronchitis is chronic bronchitis with airflow obstruction. Chronic bronchitis is defined as productive cough on most days of the week for at least 3 months total duration in 2 successive years. Chronic bronchitis becomes chronic obstructive bronchitis if spirometric evidence of airflow obstruction develops. […] Emphysema is destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar septa and radial airway traction, which increases the tendency for airway collapse. Lung hyperinflation, airflow limitation, and air trapping follow. Airspaces enlarge and may eventually develop blebs or bullae. Obliteration of small airways is thought to be the earliest lesion that precedes the development of emphysema. […] Inhalational exposures can trigger an inflammatory response in airways and alveoli that leads to disease in genetically susceptible people. The process is thought to be mediated by an increase in protease activity and a decrease in antiprotease activity. Lung proteases, such as neutrophil elastase, matrix metalloproteinases, and cathepsins, break down elastin and connective tissue in the normal process of tissue repair. Their activity is normally balanced by antiproteases, such as alpha-1 antitrypsin, airway epithelium-derived secretory leukoproteinase inhibitor, elafin, and matrix metalloproteinase tissue inhibitor. In patients with COPD, activated neutrophils and other inflammatory cells release proteases as part of the inflammatory process; protease activity exceeds antiprotease activity, and tissue destruction and mucus hypersecretion result.
  • #31 Chronic Obstructive Pulmonary Disease (COPD) – Pulmonary Disorders – MSD Manual Professional Edition
    https://www.msdmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd
    Activation of neutrophils and macrophages also leads to accumulation of free radicals, superoxide anions, and hydrogen peroxide, which inhibit antiproteases and cause bronchoconstriction, mucosal edema, and mucous hypersecretion. Neutrophil-induced oxidative damage, release of profibrotic neuropeptides (eg, bombesin), and reduced levels of vascular endothelial growth factor (VEGF) may contribute to apoptotic destruction of lung parenchyma. […] The inflammation in COPD increases as disease severity increases, and, in severe (advanced) disease, inflammation does not resolve completely despite smoking cessation. This chronic inflammation does not seem to respond to corticosteroids, particularly in patients who continue to smoke cigarettes. […] Mechanical stress on alveoli from over-distension may make them susceptible to proteases, leading to alveolar septal destruction and progressive emphysema. This is particularly notable in the upper lobes of the lung.
  • #32 Chronic Obstructive Pulmonary Disease (COPD) – Pulmonary Disorders – MSD Manual Professional Edition
    https://www.msdmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd
    The cardinal pathophysiologic feature of COPD is airflow limitation caused by airway narrowing and/or obstruction, loss of elastic recoil, or both. Airway narrowing and obstruction are caused by inflammation-mediated mucus hypersecretion, mucus plugging, mucosal edema, bronchospasm, peribronchial fibrosis, and remodeling of small airways or a combination of these mechanisms. Alveolar septa are destroyed, reducing parenchymal attachments to the airways and thereby facilitating airway closure during expiration. […] Enlarged alveolar spaces sometimes consolidate into bullae, defined as airspaces 1 cm in diameter. Bullae may be entirely empty or have strands of lung tissue traversing them in areas of locally severe emphysema; they occasionally occupy an entire hemithorax. These changes lead to loss of elastic recoil and lung hyperinflation.
  • #33 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Studies reveal that patients younger than 50 with chronic bronchitis and no airflow limitation are at increased risk of developing COPD and all-cause mortality. […] In children, initial insults, like viral infections or bacterial pneumonia, weaken the lung’s defenses, leading to excessive mucus production, reduced mucociliary clearance, and bacterial overgrowth, most likely in a biofilm. […] Environmental and genetic factors, including maternal and childhood influences, also play a key role.
  • #34 Bronchitis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bronchitis/symptoms-causes/syc-20355566
    Bronchitis is an inflammation of the lining of your bronchial tubes. These tubes carry air to and from your lungs. […] Chronic bronchitis, a more serious condition, is a constant irritation or inflammation of the lining of the bronchial tubes, often due to smoking. […] The most common cause of chronic bronchitis is cigarette smoking. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition. […] Although a single episode of bronchitis usually isn’t cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis, however, may mean that you have chronic obstructive pulmonary disease (COPD).
  • #35 Bronchitis: Types, Causes, Symptoms, and Treatment
    https://www.breathefree.com/breathing-conditions/bronchitis
    In both viral and bacterial cases, the body’s defense mechanism kicks in. The bronchial tubes then swell and produce more mucus as the body fights the infection. This swelling and mucus production narrows the airways, making breathing harder. […] With chronic bronchitis, breathing can be difficult because the lining of the airways stays swollen and produces more mucus. Chronic bronchitis can be a sign of a larger lung problem called chronic obstructive pulmonary disease (COPD). […] If your bronchitis symptoms, like coughing and fatigue, persist for several weeks and you start feeling short of breath, feverish, or experiencing chest or shoulder pain, your doctor might suspect pneumonia. Bronchitis can progress to pneumonia in anyone, but people with underlying health issues or weakened immune systems are at higher risk of serious complications. […] Acute bronchitis is often self-limiting, meaning that in most situations, it tends to improve on its own within a few weeks without needing any specific treatment. This is because the majority of bronchitis cases are caused by viruses, which antibiotics cannot treat effectively.
  • #36 Bronchitis: Symptoms, causes, treatment, and more
    https://www.medicalnewstoday.com/articles/8888
    People with bronchitis have swelling and inflammation in their bronchial tubes, the air passages that link the mouth and nose with the lungs. […] Bronchitis is a condition that affects the bronchial tubes in the lungs. They may become inflamed, resulting in symptoms such as coughing and mucus production. […] It affects the body by narrowing the airways due to swelling, meaning less air can pass through. […] Chronic bronchitis results from repeated irritation and damage to the lung and airway tissues. The most common cause is smoking, but not everyone with bronchitis is a smoker. […] Other possible causes include long term exposure to air pollution, dust, and fumes from the environment. […] The symptoms of chronic bronchitis may resolve or improve for a while. However, they will come back or become worse again, especially if there is exposure to smoke or other triggers. […] Chronic bronchitis is an ongoing condition. If a person smokes and continues to smoke, they may develop worsening symptoms, emphysema, and COPD. All these conditions can be life threatening.
  • #37 Bronchitis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bronchitis/symptoms-causes/syc-20355566
    Bronchitis is an inflammation of the lining of your bronchial tubes. These tubes carry air to and from your lungs. […] Chronic bronchitis, a more serious condition, is a constant irritation or inflammation of the lining of the bronchial tubes, often due to smoking. […] The most common cause of chronic bronchitis is cigarette smoking. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition. […] Although a single episode of bronchitis usually isn’t cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis, however, may mean that you have chronic obstructive pulmonary disease (COPD).
  • #38 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Studies reveal that patients younger than 50 with chronic bronchitis and no airflow limitation are at increased risk of developing COPD and all-cause mortality. […] In children, initial insults, like viral infections or bacterial pneumonia, weaken the lung’s defenses, leading to excessive mucus production, reduced mucociliary clearance, and bacterial overgrowth, most likely in a biofilm. […] Environmental and genetic factors, including maternal and childhood influences, also play a key role.
  • #39 Acute bronchitis in adults – UpToDate
    https://www.uptodate.com/contents/acute-bronchitis-in-adults
    Acute bronchitis is a common clinical condition characterized by an acute onset but persistent cough, with or without sputum production. It is typically self-limited, resolving within one to three weeks. Symptoms result from inflammation of the lower respiratory tract and are most frequently due to viral infection. […] Treatment is focused on patient education and supportive care. Antibiotics are not needed for the great majority of patients with acute bronchitis but are greatly overused for this condition. Reducing antibiotic use for acute bronchitis is a national and international health care priority. […] Acute bronchitis is a lower respiratory tract infection involving the large airways (bronchi), without evidence of pneumonia, that occurs in the absence of chronic obstructive pulmonary disease.
  • #40 Acute Bronchitis | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/1001/p560.html
    The primary diagnostic consideration in patients with suspected acute bronchitis is ruling out more serious causes of cough, such as asthma, exacerbation of chronic obstructive pulmonary disease, heart failure, or pneumonia. The diagnoses that have the most overlap with acute bronchitis are upper respiratory tract infections and pneumonia. […] Supportive care and symptom management are the mainstay of treatment for acute bronchitis. The role of antibiotics is limited. Since 2005, the National Committee for Quality Assurance has recommended avoidance of antibiotic prescribing for acute bronchitis as a Healthcare Effectiveness Data and Information Set Measure. All major guidelines on bronchitis, including those from the American College of Chest Physicians, recommend against using antibiotics for acute bronchitis unless the patient has a known pertussis infection.
  • #41 CSA Medical Announces Completion of Enrollment in Mechanism of Action Study utilizing the RejuvenAir® System for COPD Patients with Chronic Bronchitis – RejuvenAir
    https://rejuvenair.com/csa-medical-announces-completion-of-enrollment-in-mechanism-of-action-study-utilizing-the-rejuvenair-system-for-copd-patients-with-chronic-bronchitis/
    CSA Medical, Inc., today announced that all subjects have been enrolled in the RejuvenAir System study Characterizing the Mechanism of Action of Metered Cryospray for the Treatment of Patients with Chronic Obstructive Pulmonary Disease with Chronic Bronchitis. The aim of this study is to determine the mechanism by which Metered CryoSpray (MCS) reduces the density of goblet cells responsible for over-producing mucus and observe re-growth of healthy cilia in the airways. […] What makes this study different is that we will now be able to provide the cellular rationale for the remodeling response we observed in the feasibility study after treatment with RejuvenAir. In other words, we will prove re-epithelialization and regrowth of healthy airway tissue. […] Together with the final data from the SPRAY-CB pivotal study, we endeavor to understand metered cryospray not only reduces the symptoms of chronic bronchitis, but also how it works to rejuvenate airways for a better quality of life. […] It is anticipated that the rapid freezing of the epithelial layer of the airway walls will destroy the damaged cilia and mucus-producing goblet cells while preserving the extracellular matrix, thereby enabling the regrowth of healthy cells.
  • #42 Exploring the mechanism of Lianhuaqingwen (LHQW) in treating chronic bronchitis based on network pharmacology and experimental validation | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-02927-7
    Lianhuaqingwen (LHQW) has been used in the treatment of chronic bronchitis, but the precise mechanism through which LHQW exhibits its anti-inflammatory effects in this context is not yet fully understood. […] The development of chronic bronchitis is a multifaceted process influenced by the intricate regulation of numerous genes and proteins. […] LHQW possesses anti-inflammatory properties by suppressing cytokine responses, which may help in addressing chronic bronchial inflammation and reducing lung injury. […] By constructing a protein-protein interaction (PPI) network for the 76 potential gene targets, four core targets (TNF, IL6, IFNG, and STAT3) were identified as primarily involved in responses to lipopolysaccharide, the TNF pathway, and the JAK-STAT pathway. […] Molecular docking results revealed a favorable affinity between multiple active ingredients of LHQW and the four core targets, suggesting that the therapeutic effects are mediated through the inhibition of inflammatory responses and signaling pathways.
  • #43 Exploring the mechanism of Lianhuaqingwen (LHQW) in treating chronic bronchitis based on network pharmacology and experimental validation | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-02927-7
    LHQW shows multi-active ingredients interacting with multiple targets to treat chronic bronchitis. […] Quercetin, a polyphenolic flavonoid present in LHQW, displays a strong interaction with TNF, IL6, IFNG, and STAT3, highlighting its potential as a crucial active ingredient of LHQW. […] Our findings indicate that LHQW enhances cell viability and colony formation in LPS-induced 16HBE cells while concurrently reducing the expression levels of TNF-, IL6, and IFNG and inhibiting the JAK-STAT pathway. […] These enrichment findings suggest that gene targets are mainly associated with chronic bronchitis development and progression.
  • #44 Acute Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK448067/
    Acute bronchitis is characterized by inflammation in the bronchi lining, is a frequent condition in emergency departments, urgent care centers, and primary care offices. […] The etiology of these symptoms arises from the inflammatory response within the lower respiratory tract, often triggered by viral infections. […] This condition primarily impacts the bronchial tree, leading to irritation, inflammation, and increased mucus production. Viral infections, such as the common cold or influenza viruses, adenovirus, and rhinovirus, are frequent instigators, although exposure to irritants or other respiratory pathogens can also be putative triggers. […] The inflammatory process triggers increased blood flow and cellular activity within the affected bronchi, resulting in heightened 18F-fluorodeoxyglucose (FDG) uptake when observed via positron-emission tomography (PET) scan.
  • #45 Chronic Bronchitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482437/
    Chronic bronchitis is a long-term inflammatory condition of the airways, characterized by a persistent productive cough without other identifiable underlying causes lasting at least 3 months per year for 2 consecutive years. […] Chronic bronchitis leads to excessive mucus production, causing airway obstruction and inflammation. […] Goblet cell hyperplasia leads to excessive mucus production. This, combined with reduced mucus clearance, causes airway inflammation, structural changes, and obstruction. […] In adults with chronic bronchitis, cigarette smoke exposure, recurrent or chronic viral and bacterial infections, or toxic environmental exposures stimulate mucus overproduction and hypersecretion, and inflammatory and humoral mediators stimulate the release of mucin to protect the airway against noxious stimuli.
  • #46 Exploring the mechanism of Lianhuaqingwen (LHQW) in treating chronic bronchitis based on network pharmacology and experimental validation | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-02927-7
    Lianhuaqingwen (LHQW) has been used in the treatment of chronic bronchitis, but the precise mechanism through which LHQW exhibits its anti-inflammatory effects in this context is not yet fully understood. […] The development of chronic bronchitis is a multifaceted process influenced by the intricate regulation of numerous genes and proteins. […] LHQW possesses anti-inflammatory properties by suppressing cytokine responses, which may help in addressing chronic bronchial inflammation and reducing lung injury. […] By constructing a protein-protein interaction (PPI) network for the 76 potential gene targets, four core targets (TNF, IL6, IFNG, and STAT3) were identified as primarily involved in responses to lipopolysaccharide, the TNF pathway, and the JAK-STAT pathway. […] Molecular docking results revealed a favorable affinity between multiple active ingredients of LHQW and the four core targets, suggesting that the therapeutic effects are mediated through the inhibition of inflammatory responses and signaling pathways.
  • #47 Lung macrophages drive mucus production and steroid-resistant inflammation in chronic bronchitis | Respiratory Research | Full Text
    https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01762-4
    We hypothesized that the highly neutrophilic and pro-inflammatory cytokine milieu in sputum plugs may drive development of a steroid-resistant, chronically activated macrophage phenotype that constantly secretes inflammatory signals driving mucus hyper-production by epithelial cells. […] Given the importance of TNF as mediator in the mechanistic macrophage-epithelial cross-talk assay and the chronic TNF expression observed in the clinically sampled sputum macrophages, the effect of the corticosteroid dexamethasone was investigated by measuring the amount of TNF protein released into the media of ex vivo cultured sputum and alveolar macrophages. […] Taken together, these data show that, in contrast to alveolar macrophages from either COPD or non-COPD donors, sputum macrophages from COPD chronic bronchitis patients are steroid resistant. […] In conclusion, our data pinpoint a critical role for sputum macrophages in chronic bronchitis by perpetuating macrophage-epithelial signaling that can drive aberrant mucin expression in bronchial epithelial cells.