哺乳动物粘膜屏障分泌抗菌肽（AMP）作为微生物群的关键、宿主衍生的调节剂。然而，支持微生物群稳态响应炎症刺激（例如超生理氧）的机制仍不清楚。我们发现，新生小鼠的超生理氧暴露，或肠道类器官直接暴露于超生理氧，会抑制肠道 AMP 的表达并改变肠道微生物群组成。给暴露于高氧的新生小鼠口服补充原型 AMP 溶菌酶可减少高氧诱导的微生物群变化，并与减少肺损伤相关。我们的结果确定了由肠道 AMP 表达驱动并由肠道微生物群介导的肠肺轴，即与新生儿肺损伤有关。总之，这些数据支持肠道 AMP 调节肺损伤和修复。视频摘要。© 2023。BioMed Central Ltd.，Springer Nature 的一部分。

Mammalian mucosal barriers secrete antimicrobial peptides (AMPs) as critical, host-derived regulators of the microbiota. However, mechanisms that support microbiota homeostasis in response to inflammatory stimuli, such as supraphysiologic oxygen, remain unclear.We show that supraphysiologic oxygen exposure to neonatal mice, or direct exposure of intestinal organoids to supraphysiologic oxygen, suppresses the intestinal expression of AMPs and alters intestinal microbiota composition. Oral supplementation of the prototypical AMP lysozyme to hyperoxia-exposed neonatal mice reduced hyperoxia-induced alterations in their microbiota and was associated with decreased lung injury.Our results identify a gut-lung axis driven by intestinal AMP expression and mediated by the intestinal microbiota that is linked to lung injury in newborns. Together, these data support that intestinal AMPs modulate lung injury and repair. Video Abstract.© 2023. BioMed Central Ltd., part of Springer Nature.