Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?

Abstract

Lingappan K, Moorthy B. Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?. Am J Physiol Lung Cell Mol Physiol 309: L1383-L1386, 2015. First published September 11, 2015 doi:10.1152/ajplung.00313.2015The effect of adverse perinatal environment (like maternal infection) has long-standing effects on many organ systems, including the respiratory system. Use of maternal nutritional supplements is an exciting therapeutic option that could be used to protect the developing fetus. In a recent issue of the journal, Ali and associates (Ali M, Heyob KM, Velten M, Tipple TE, Rogers LK. Am J Physiol Lung Cell Mol Physiol 309: L441-L448, 2015) specifically look at maternal docosahexaenoic acid (DHA) supplementation and its effect on chronic apoptosis in the lung in a mouse model of perinatal inflammation and postnatal hyperoxia. Strikingly, the authors show that pulmonary apoptosis was augmented even 8 wk after the hyperoxiaexposed mice had been returned to room air. This effect was significantly attenuated in mice that were subjected to maternal dietary DHA supplementation. These findings are novel, significantly advance our understanding of chronic effects of adverse perinatal and neonatal events on the developing lung, and thereby offer novel therapeutic options in the form of maternal dietary supplementation with DHA. This editorial reviews the long-term effects of adverse perinatal environment on postnatal lung development and the protective effects of dietary supplements such as DHA. docosahexaenoic acid; hyperoxia MATERNAL INFLAMMATION DURING pregnancy can occur by intraor extrauterine processes. Maternal infections both systemic (urinary tract infection, periodontitis) and chorioamnionitis have been associated with premature birth (17,27,36,49). Chorioamnionitis leads to fetal lung inflammation in animal models (18,28). The clinical correlation between chorioamnionitis and development of bronchopulmonary dysplasia (BPD) is not strong, with evidence being available both for and against the association (19,41). In animal models, chorioamnionitis induces lung maturation (increase in surfactant proteins) but also causes delayed alveolarization and vascular injury (15, 18). Intra-amniotic lipopolysaccharide (LPS) on embryonic day 15 increases alveolar type II cell number through Toll-like receptor-4 signaling (33). Maternal inflammation can potentially initiate the inflammatory cascade in the fetal lung, which can be further potentiated by postnatal exposures such as hyperoxia (45). Antenatal corticosteroids (maternal ␤-methasone) given to pregnant ewes decrease intrauterine inflammation-induced TGF-␤ signaling in fetal lungs (9). Cao et al. showed that maternal exposure to systemic endotoxin in pregnant rats increases pulmonary inflammation in the pups, altered gene expression of molecules involved in alveologenesis, and delayed morphological maturation (6). Salminen et al. found that, following systemic maternal endotoxin administration, the inflammatory signal is rapidl...

Recent advances in our understanding of the mechanisms of late lung development and bronchopulmonary dysplasia

“…This is noteworthy given the recent report that HMGB1 contributes causally to arrested lung alveolarization in experimental BPD (583). No doubt, the use of DHA supplementation to promote proper structural development of the lung will continue to be explored (302).…”