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The airway surface liquid (ASL) is a complex, two-layer fluid system covering the respiratory epithelium, comprising an underlying periciliary liquid (PCL) layer and an overlying mucus gel layer [1]. Its primary biological function is mucociliary clearance, where the mucus traps inhaled particles and pathogens while the PCL provides a low-friction environment for ciliary beating to transport the mucus out of the lungs [2]. In pathological states such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD), dysregulation of ion transport (e.g., via CFTR or ENaC) leads to ASL dehydration, resulting in thick, stagnant mucus that promotes chronic infection and inflammation [3]. Pharmacological strategies targeting the ASL include osmotic agents like hypertonic saline to increase hydration, mucolytics like N-acetylcysteine to break down mucus structure, and nucleases like dornase alfa to reduce viscosity caused by extracellular DNA [4]. Although the ASL is a physiological compartment rather than a single protein, it is a central focus for therapies aimed at restoring respiratory hygiene and lung function [5]. Sources: [1] Boucher, R. C. (2007). Evidence for airway surface liquid dehydration as the initiating event in CF lung disease. Journal of Internal Medicine. [2] Fahy, J. V., & Dickey, B. F. (2010). Airway mucus function and dysfunction. New England Journal of Medicine. [3] NIH/StatPearls: Cystic Fibrosis. [4] FDA: Pulmozyme (dornase alfa) Prescribing Information. [5] PubChem: Hypertonic Saline.
Osmotic hydration of the airway surface, enzymatic degradation of extracellular DNA, and reduction of mucin disulfide bonds to decrease viscosity.
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