Bronchial mucus secretion

Bronchial mucus secretion is a complex physiological process in the lungs where goblet cells and submucosal glands produce and release a viscoelastic gel to protect the airway epithelium [3, 6]. This mucus layer acts as a primary host defense mechanism, facilitating the mucociliary escalator to trap and remove inhaled pathogens, allergens, and particulates [2, 12]. In chronic respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD), this process is dysregulated, leading to mucus hypersecretion and the formation of obstructive mucus plugs [4, 5, 10]. Secretion is regulated by various factors, including vagal cholinergic stimulation of muscarinic M3 receptors, inflammatory cytokines such as IL-13, and secretagogues like neutrophil elastase [1, 15, 17]. Therapeutic interventions aim to reduce hypersecretion using anticholinergics (e.g., tiotropium), leukotriene antagonists (e.g., montelukast), and corticosteroids, or to facilitate clearance using mucolytic agents like acetylcysteine that degrade the glycoprotein matrix [4, 13, 16]. Emerging therapies also target the intracellular exocytotic machinery, such as the MARCKS protein, to specifically block the release of mucin granules [2].

Other names

Airway mucus hypersecretionMucus hypersecretionBronchial hypersecretionSputum productionAirway mucus secretion

Drugs modulate bronchial mucus secretion by antagonizing muscarinic M3 receptors to block secretomotor signaling, inhibiting leukotriene receptors, suppressing Th2-driven inflammatory cytokine production, inhibiting MARCKS-mediated mucin granule exocytosis, or chemically disrupting disulfide bonds in mucin glycoproteins to reduce viscosity.