Depressed exocytosis and endocytosis of type II alveolar epithelial cells are responsible for the surfactant deficiency in the lung of newborn with congenital diaphragmatic hernia

Abstract

Exocytosis and endocytosis are the way of macromolecules transmembrane transport. Pulmonary surfactant (PS), one of such macromolecules, is secreted via exocytosis of lamellar bodies and recycled via endocytosis by type II alveolar epithelial cells (AEC II). It maintains low alveolar surface tension and is therefore essential to normal lung function. PS deficiency causes respiratory distress syndrome in infants. Congenital diaphragmatic hernia is an abnormal condition in which low lung compliance is involved. This condition is multifactorial and a primary surfactant deficiency may be responsible for it. We hypothesize that surfactant deficiency is involved in CDH and depressed activity of exocytosis and endocytosis in AEC II is responsible for the surfactant deficiency in the lung of newborn with congenital diaphragmatic hernia.