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Lung epithelial cells undergo apoptosis in neonatal respiratory distress syndrome
Heikki P Lukkarinen1, Jukka Laine, Pekka O Kääpä
1Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. heikki.lukkarinen@utu.fi
Insights
Programmed cell death (apoptosis) is present in the lungs of infants with fatal respiratory distress syndrome (RDS). Postnatal dexamethasone treatment reduced this lung epithelial apoptosis in infants with RDS.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Cell Biology
Background:
- Respiratory distress syndrome (RDS) is a significant cause of mortality in premature infants.
- Programmed cell death, or apoptosis, is a critical cellular process that can contribute to tissue injury.
- The role of apoptosis in the pathogenesis of fatal RDS and the impact of postnatal steroid therapy require further investigation.
Purpose of the Study:
- To investigate the presence and extent of programmed cell death in the lungs of infants with fatal RDS.
- To determine the potential influence of postnatal glucocorticoid administration on lung cell apoptosis in these infants.
Main Methods:
- Autopsy lung tissue samples were analyzed from 16 premature infants with fatal RDS and control neonates.
- Histological examination was performed to assess tissue injury.
- Apoptotic cell death was identified using DNA nick end-labeling assay and M30 antibody staining (CytoDeath).
Main Results:
- Infants with fatal RDS exhibited increased leukocyte infiltration, higher histological injury scores, and more apoptotic cells in lung tissue compared to controls.
- Epithelial cells were the primary location of apoptosis in RDS lungs.
- Infants with RDS who received postnatal dexamethasone showed significantly reduced leukocyte infiltration, lower injury scores, and decreased rates of epithelial apoptosis compared to those without dexamethasone treatment.
Conclusions:
- Significant epithelial apoptosis occurs in the lungs of newborn infants suffering from fatal RDS.
- Postnatal dexamethasone administration may attenuate lung epithelial apoptosis in infants with RDS, suggesting a potential therapeutic benefit.
Abstract:
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.