88 Expression of αEnac in Airways Correlates with Endogenous Cortisol in Newborn Term Infants

Abstract

Objective: Reabsorption of lung fluid is critical for the adaptation of the newborn infant. Defective reabsorption may result in transient tachypnea of the newborn or contribute to respiratory distress syndrome. Perinatally, epithelial sodium channel (ENaC) is crucial for lung fluid reabsorption. ENaC is composed of 3 homologous subunits, the α-subunit being indispensable to ENaC function. Exogenous glucocorticoids (GC) regulate ENaC gene expression, but little is known whether an association exists between endogenous cortisol and ENaC. Subjects and methods: 69 term infants delivered vaginally (n=22) or by elective cesarean section (CS) (n=47) were included. We collected cord blood and saliva for cortisol analyzes with ELISA. Airway epithelium ENaC mRNA was quantified with real-time RT-PCR and normalized to cytokeratin 18 (CK18). Saliva and airway epithelial sampling was performed < 3h, 24 ± 5 and 48 ± 8 h postnatally. In a subset of infants delivered by elective CS (n = 26) first airway samples were obtained < 30 min postnatally. Results: αENaC mRNA < 30 min postnatally correlated with cord cortisol; r = 0.64, p = 0.001 (n=22). Adjusted for GA the correlation remained significant; r = 0.59, p = 0.005. At < 3h postnatally αENaC correlated with salivary cortisol; r = 0.52, p = 0.004 (n=29). Conclusion: Cortisol seems to be an important physiologic regulator of ENaC expression at birth. Our finding suggests that lung fluid transport may respond to GC even in the term infant. This underlines the potentials of regulation of perinatal lung fluid reabsorption by GC.