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Chronic bronchitis, a major phenotype of COPD, results from prolonged exposure to airborne irritants such as cigarette smoke.
These irritants trigger persistent inflammation that begins in the larger bronchi and extends into the smaller airways.
Neutrophils, macrophages, and lymphocytes infiltrate the bronchial walls, causing epithelial injury.
Inflammation also causes squamous metaplasia, which replaces the ciliated epithelium with squamous cells, impairing mucociliary clearance.
Meanwhile, goblet cells and submucosal glands undergo hyperplasia and hypertrophy, producing thick mucus that clogs the airways and promotes infection.
Persistent inflammation and mucus plugging lead to airway remodeling, including smooth muscle hypertrophy and fibrosis, which narrow the airways, especially during expiration.
Airway obstruction creates a ventilation–perfusion mismatch, leading to hypoxemia. Progressive air trapping causes hyperinflation, which flattens the diaphragm, reduces ventilatory efficiency, and increases the work of breathing.
Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overpro…
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