Inhaled oxygen, although commonly administered to patients with respiratory disease, causes severe lung injury in animals and is associated with poor clinical outcomes in humans. The relationship between hyperoxia, lung and gut microbiota, and lung injury is unknown. Here, we show that hyperoxia conferred a selective relative growth advantage on oxygen-tolerant respiratory microbial species (e.g., Staphylococcus aureus) as demonstrated by an observational study of critically ill patients receiving mechanical ventilation and experiments using neonatal and adult mouse models. During exposure of mice to hyperoxia, both lung and gut bacterial communities were altered, and these communities contributed to oxygen-induced lung injury. Disruption of lung and gut microbiota preceded lung injury, and variation in microbial communities correlated with variation in lung inflammation. Germ-free mice were protected from oxygen-induced lung injury, and systemic antibiotic treatment selectively modulated the severity of oxygen-induced lung injury in conventionally housed animals. These results suggest that inhaled oxygen may alter lung and gut microbial communities and that these communities could contribute to lung injury.

吸入氧气虽然通常用于呼吸系统疾病患者，但会导致动物严重肺损伤，并与人类不良的临床结果相关。高氧、肺和肠道微生物群以及肺损伤之间的关系尚不清楚。在这里，我们表明高氧对耐氧呼吸道微生物物种（例如金黄色葡萄球菌）赋予了选择性的相对生长优势。）正如一项对接受机械通气的危重患者的观察性研究和使用新生儿和成年小鼠模型的实验所证明的那样。在小鼠暴露于高氧期间，肺和肠道细菌群落都发生了改变，这些群落导致氧诱导的肺损伤。肺和肠道微生物群的破坏先于肺损伤，微生物群落的变化与肺部炎症的变化相关。无菌小鼠免受氧诱导的肺损伤，全身抗生素治疗选择性地调节常规饲养动物的氧诱导肺损伤的严重程度。这些结果表明，吸入氧气可能会改变肺和肠道微生物群落，并且这些群落可能导致肺损伤。