Dexamethasone and epinephrine stimulate surfactant secretion in type II cells of embryonic chickens

Pulmonary surfactant (PS), a mixture of phospholipids and proteins secreted by alveolar type II cells, functions to reduce the surface tension in the lungs of all air-breathing vertebrates. Here we examine the control of PS d uring lung development in a homeothermic egg-laying vertebrate. In mammals, glucocorticoids and autonomic neurotransmitters contribute to the maturati on of the surfactant. system. We examined whether dexamethasone, epinephrin e, and carbamylcholine hydrochloride (agonist for acetylcholine) increased the amount of PS secreted from cultured type II cells of the developing chi cken lung. In particular, we wanted to establish whether dexamethasone woul d increase PS secretion through a process involving lung fibroblasts. We is olated and cocultured type II cells and lung fibroblasts from chickens afte r 16, 18, and 20 days of incubation and from hatchlings (day 21). Epinephri ne stimulated phosphatidylcholine (PC) secretion at all stages, whereas dex amethasone stimulated secretion of PC at days 16 and 18. Carbamylcholine hy drochloride had no effect at any stage. This is the first study to establis h the existence of similar cellular pathways regulating the development of surfactant in chickens and eutherian mammals, despite the vastly different birthing strategies and lung structure and function.