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1 Pediatrics, Yale University School of Medicine, New Haven, Connecticut, United States
2 Pathology, Yale University School of Medicine, New Haven, Connecticut, United States
3 Internal Medicine, Yale University School of Medcine, New Haven, Connecticut, United States
* To whom correspondence should be addressed. E-mail: vineet.bhandari{at}yale.edu.
Rationale: Our previous work has shown that adult mice with overexpression of IL-6 and IL-13 in the lung have enhanced survival in hyperoxia associated with reduced hyperoxia-induced lung injury (HALI) and cell death. Objectives: We hypothesized that there are developmental differences in these responses in the adult versus the newborn (NB) animal, and these responses have clinical relevance in the human NB. Methods: We compared the responses to 100% O2 of NB IL-6 and IL-13 transgenic mice with wild-type (WT) litter-mate controls by evaluating mortality, lung tissue TUNEL staining, and mRNA expression using RT-PCR. We used ELISA to measure IL-6 levels in tracheal aspirates from human neonates. Measurements and Main Results: Our results show that, in contrast to the cytoprotective effects in mature mice, IL-6 caused significantly increased mortality, DNA injury, caspases, cell death regulators and angiogenic factors expression in hyperoxia in the NB. Furthermore, tracheal aspirate levels of IL-6 were significantly increased in premature neonates with respiratory distress syndrome who had an adverse outcome (bronchopulmonary dysplasia/death). In contrast to the protective effects in adults, there was no survival advantage to the NB IL-13 mice in hyperoxia. Conclusion: These findings imply that caution should be exercised in extrapolating results from the adult to the NB.
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