Lung epithelial cells undergo apoptosis in neonatal respiratory distress syndrome.

For studying the presence of programmed cell death in the lungs of infants with fatal respiratory distress syndrome (RDS) and the possible contribution of postnatal glucocorticoid administration on this cell destruction, lung tissue samples from autopsies of 16 premature infants with fatal RDS were studied. The infants had neither been exposed to antenatal steroids nor received surfactant therapy, but seven of these infants had been subjected to postnatal dexamethasone treatment. Lung autopsy samples of seven term and two preterm neonates without any obvious lung disease served as controls. Lungs were studied histologically, and apoptotic cell death was identified using DNA nick end-labeling assay and caspase-related M30 antibody staining (CytoDeath). Lung tissue from the RDS infants showed elevated leukocyte infiltration, histologic injury score, and number of apoptotic cells, located mainly in the respiratory epithelium, when compared with controls. In contrast, lungs from infants who had RDS and received dexamethasone demonstrated markedly reduced tissue leukocyte accumulation and injury score and lower rates of epithelial apoptosis than the lungs of infants who had RDS and did not receive dexamethasone. These results suggest that significant epithelial apoptosis is present in the lungs of newborn infants with fatal RDS and that this apoptosis may be attenuated by steroid administration.