Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD
نویسندگان
چکیده
The airway epithelium comprises of different cell types and acts as a physical barrier preventing pathogens, including inhaled particles microbes, from entering the lungs. Goblet cells submucosal glands produce mucus that traps which are expelled respiratory tract by ciliated cells. Basal act progenitor cells, differentiating into epithelial types, to maintain homeostasis following injury. Adherens tight junctions between function regulate movement molecules across it. In this review we discuss how abnormal structure function, caused chronic injury repair, drives disease specifically asthma obstructive pulmonary (COPD). both diseases, allergens, pollutants microbes disrupt junctional complexes promote death, impairing leading increased penetration pathogens constant immune response. asthma, inflammatory response precipitates basal differentiation. This leads reduced goblet hyperplasia mesenchymal transition, contribute impaired mucociliary clearance remodelling. COPD, oxidative stress inflammation trigger premature senescence, contributes loss integrity Increased numbers showing deregulated differentiation, ciliary dysfunction mucous hyperproduction in COPD airways. Defective antioxidant, antiviral damage repair mechanisms, possibly due genetic or epigenetic factors, may confer susceptibility these diseases. current evidence suggests cycle remodelling COPD. Mechanistic understanding lead improved therapies for
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ژورنال
عنوان ژورنال: Frontiers in Immunology
سال: 2023
ISSN: ['1664-3224']
DOI: https://doi.org/10.3389/fimmu.2023.1201658