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Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD
Summary
This review examines how air pollutants including particulate matter, ozone, and cigarette smoke damage the protective lining of the airways, contributing to asthma and COPD. Researchers found that these pollutants disrupt the physical barrier of airway cells, trigger excessive inflammation, and alter the lung microbiome, all of which can worsen respiratory disease. The study suggests that understanding these barrier-disruption mechanisms could lead to new treatments for restoring airway integrity.
Chronic exposure to environmental pollutants is a major contributor to the development and progression of obstructive airway diseases, including asthma and COPD. Understanding the mechanisms underlying the development of obstructive lung diseases upon exposure to inhaled pollutants will lead to novel insights into the pathogenesis, prevention and treatment of these diseases. The respiratory epithelial lining forms a robust physicochemical barrier protecting the body from inhaled toxic particles and pathogens. Inhalation of airborne particles and gases may impair airway epithelial barrier function and subsequently lead to exaggerated inflammatory responses and airway remodelling, which are key features of asthma and COPD. In addition, air pollutant-induced airway epithelial barrier dysfunction may increase susceptibility to respiratory infections, thereby increasing the risk of exacerbations and thus triggering further inflammation. In this review, we discuss the molecular and immunological mechanisms involved in physical barrier disruption induced by major airborne pollutants and outline their implications in the pathogenesis of asthma and COPD. We further discuss the link between these pollutants and changes in the lung microbiome as a potential factor for aggravating airway diseases. Understanding these mechanisms may lead to identification of novel targets for therapeutic intervention to restore airway epithelial integrity in asthma and COPD.
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