Zhang Meiyu, Li Decai, Sun Liujuan, He Yu, Liu Qingqing, He Yi, Li Fang
National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Department of Neonatology Children's Hospital of Chongqing Medical University, Chongqing 400015, China.
Department of Pediatrics Chongqing Health Center for Women and Children, Department of Pediatrics Women and Children's Hospital of Chongqing Medical University, Chongqing 401147, China.
Mediators Inflamm. 2024 Dec 9;2024:4965271. doi: 10.1155/mi/4965271. eCollection 2024.
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.
支气管肺发育不良（BPD）是早产儿最常见的慢性呼吸道疾病。关于肺在BPD中的调节作用及其机制知之甚少。本研究探讨了[具体物质未给出]对高氧诱导的小鼠肺损伤的影响，并检测了[具体物质未给出]是否通过IL-22/STAT3途径发挥作用。我们发现经鼻给予[具体物质未给出]及其色氨酸代谢产物吲哚-3-醛（3-IAld）可改善高氧诱导的小鼠肺BPD样改变，降低促炎细胞因子（IL-1、IL-6和TNF-）水平，并提高表面活性物质相关蛋白C（SPC）、水通道蛋白5（AQP5）和血管内皮生长因子受体2（VEGFR2，也称为FLK-1）的水平。此外，[具体物质未给出]和3-IAld增加了IL-22的表达。IL-22也被证实可改善高氧诱导的小鼠肺病理变化，并且[具体物质未给出]的保护作用可被抗IL-22中和抗体抑制。最后，我们在MLE-12细胞中证实了IL-22对STAT3的激活作用。总之，我们的研究证实[具体物质未给出]通过IL-22的产生激活IL-22/STAT3信号通路，减轻了高氧诱导的小鼠肺BPD样改变。益生菌[具体物质未给出]是新生儿高氧诱导肺损伤的一种潜在治疗方法。
