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The alveolar lipid monolayer is a specialized lipid film formed primarily from pulmonary surfactant at the air–liquid interface of alveoli. It is produced mainly by type 2 alveolar epithelial cells and composed of approximately 90% lipids (predominantly phosphatidylcholine, especially dipalmitoyl phosphatidylcholine, with smaller fractions of phosphatidylglycerol, phosphatidylinositol, cholesterol, sphingolipids, and plasmalogens) and 10% surfactant proteins. This monolayer reduces surface tension at the alveolar surface, preventing alveolar collapse upon expiration and facilitating efficient gas exchange. Structural integrity and surface activity depend on the precise lipid composition and organization. Although alterations in surfactant lipids are critical in many lung diseases, the monolayer itself is not a traditional molecular therapeutic target (e.g., not a receptor, enzyme, or channel), but rather a functional biomaterial interface essential for respiration. Disturbances of its composition or function underlie several pulmonary pathologies and are treated with exogenous surfactant therapies[1][5][6].
Surface tension reduction (by forming a lipid monolayer at the air–liquid interface); Modulation of innate immune responses (by surfactant lipids influencing alveolar macrophage function)
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