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Airway mucosal cells represent a heterogeneous population of specialized cells, including ciliated, goblet, and basal cells, that line the respiratory tract and serve as a critical interface between the host and the environment [9, 12, 15]. Their primary biological function involves maintaining a protective physicochemical barrier through the production of a complex mucus gel and the execution of mucociliary clearance to remove inhaled pathogens and irritants [1, 8, 24]. In chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis, these cells undergo structural and functional remodeling, characterized by goblet cell hyperplasia, impaired barrier integrity, and dysregulated cytokine secretion [2, 5, 7, 20]. Therapeutic interventions interacting with airway mucosal cells focus on modulating mucus production, enhancing clearance, or restoring epithelial integrity to alleviate airway obstruction and reduce inflammation [3, 4, 22]. While several mucoactive and anti-inflammatory drugs target proteins expressed within these cells, the term describes a broad cellular population rather than a specific molecular target [11, 13, 21].
Drugs interacting with airway mucosal cells typically function by modulating the viscoelastic properties of mucus (mucolytics), inhibiting rapid mucin secretion via proteins such as synaptotagmin-2, or correcting ion channel function (e.g., CFTR) to improve hydration and mucociliary clearance [3, 21, 22]. Additionally, corticosteroids and other anti-inflammatory agents suppress the release of proinflammatory cytokines and chemokines from these cells to reduce airway remodeling and tissue damage [3, 4, 5].
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