Alleviates Hyperoxia-Induced BPD by Activating IL-22/STAT3 Signaling Pathway in Neonatal Mice.

Bronchopulmonary dysplasia (BPD) is the most common chronic respiratory disease in preterm infants. Little is known about the regulatory effect of lung and its mechanism in BPD. This study explored the effect of on hyperoxia-induced mice lung injuries and examined whether played a role via the IL-22/STAT3 pathway. We found that the intranasal administration of and its tryptophan metabolite indole-3-aldehyde (3-IAld) ameliorated hyperoxia-induced mice lung BPD-like changes, deceased proinflammatory cytokines (IL-1, IL-6, and TNF-), and increased the levels of surfactant-associated protein C (SPC), aquaporin 5 (AQP5), and vascular endothelial growth factor receptor 2 (VEGFR2, also known as FLK-1). Furthermore, and 3-IAld increased the expression of IL-22. IL-22 was also confirmed to ameliorate hyperoxia-induced mice lung pathological changes, and the protective effects of could be inhibited by anti-IL-22 neutralizing antibody. Finally, we confirmed STAT3 activation by IL-22 in MLE-12 cells. In summary, our study confirmed alleviated hyperoxia-induced lung BPD-like changes in mice by activating the IL-22/STAT3 signaling pathway via IL-22 production. Probiotics is a potential treatment for hyperoxia-induced lung injury in newborns.