Maternal Lactobacillus johnsonii supplementation attenuates hyperoxia-induced lung injury in neonatal mice through microbiota regulation.

Abstract

Background: Supplemental oxygen impairs lung development in premature infants with respiratory distress. This study investigated the effects of maternal Lactobacillus johnsonii supplementation on hyperoxia-induced lung injury in neonatal mice.

Methods: Pregnant C57BL/6 mice received L. johnsonii in normal saline (NS) from gestational days 16-21. Control pregnant mice received an equal volume of NS. After birth, the pups were exposed to hyperoxia (O₂) or room air (RA) for 1 week. Four groups were studied: NS + RA, probiotic + RA, NS + O₂, and probiotic + O₂. On postnatal day 7, the lung and intestinal microbiota were sampled, and the right lung was analyzed.

Results: Compared to the NS + RA, probiotic + RA, and probiotic + O₂ groups, the NS + O₂ group exhibited significantly lower body weight, lung vascular density, and more significant mean linear intercept, IL-6, and 8-OHdG. In the genus level of gut microbiota, the NS + O₂ group showed considerably more Staphylococcus and less Lactobacillus than the other three groups. The outcomes showed that in neonatal mice exposed to hyperoxia, maternal L. johnsonii supplementation improved lung development, decreased IL-6 and 8-OHdG levels, and restored gut microbiota.

Conclusions: Maternal L. johnsonii supplementation reduced lung inflammation and improved lung development in hyperoxia-exposed neonatal mice. The mechanism may be related to the gut microbiota, as L. johnsonii improved gut microbiota communities and regulated dysregulated metabolic pathways.