Surfactant metabolism

The alveolar region of the lung creates an extensive epithelial surface that mediates the transfer of oxygen and carbon dioxide required for respiration after birth. Type I epithelial cells form the alveolar surface and mediate gaseous exchange. Type II epithelial cells secrete pulmonary surfactant, a lipoprotein complex that forms a thin interfacial film, lowering surface tension at the air-liquid interface in alveoli and maintaining the structural integrity of alveoli, preventing their collapse at low volumes. Surfactant production is increased prior to birth, in preparation for air breathing at birth. Pre-term infants, where type II epithelial cells are not fully differentiated yet, can produce insufficient surfactant and result in respiratory distress syndrome. Surfactant is composed primarily of phospholipids enriched in phosphatidylcholine (PC) and phosphatidylglycerol (PG) and the pulmonary collectins, termed surfactant proteins A, B, C and D (SFTPA-D). They influence surfactant homeostasis, contributing to the physical structures of lipids in the alveoli and to the regulation of surfactant function and metabolism. They are directly secreted from alveolar type II cells into the airway to function as part of the surfactant. SFTPA and D are large, hydrophilic proteins while SFTPB and C are small, very hydrophobic proteins. In addition to their surfactant functions, SFTPA and D play important roles in innate host defense by binding and clearing invading microbes from the lung. Nuclear regulation, transport, metabolism, reutilisation and degradation of surfactant are described here. Mutations in genes involved in these processes can result in respiratory distress syndrome, lung proteinosis, interstitial lung diseases and chronic lung diseases.

Summary from Reactome (R-HSA-5683826), read 2026-09-23.