Gut microbiota mediate the protective effects on endometritis induced byStaphylococcus aureusin mice
Gut microbiota mediate the protective effects on endometritis induced byStaphylococcus aureusin mice
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肠道菌群介导对金黄色葡萄球菌引起的小鼠子宫内膜炎的保护作用
DOI：
10.1039/c9fo02963j
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发表时间：
2020-04-01
期刊：
影响因子：
6.1
通讯作者：
Fu, Yunhe
中科院分区：
文献类型：
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作者：
Hu, Xiaoyu;Mu, Ruiying;Fu, Yunhe
子宫内膜炎是由细菌性病原体引起的子宫内膜炎症，与生殖障碍有关。近年来的研究表明，肠道菌群在感染性疾病中起着重要作用。然而，肠道菌群在子宫内膜炎中的作用仍不清楚。在本文中，我们评估了在金黄色葡萄球菌（S。 aureus)具有良好的抗菌活性。用抗生素混合物（Abx）建立小鼠肠道菌群失调模型，再用沙门氏菌（S.通过粪便微生物移植（FMT）来评估肠道微生物与子宫内膜炎的关系。结果表明，肠道菌群失调小鼠出现子宫炎症反应，而FMT可减轻肠道菌群失调小鼠的子宫炎症反应。此外，S.金黄色葡萄球菌诱导的子宫内膜炎在具有肠道生态失调的小鼠中的严重程度比未治疗的小鼠更高。此外，FMT可逆转小鼠肠道菌群失调。GC-MS分析表明，肠道菌群失调小鼠粪便中短链脂肪酸（SCFAs）水平显著降低，丁酸钠或丙酸钠预处理提高了循环和子宫组织中丁酸或丙酸的浓度，从而减轻了S.金黄色。此外，肠道菌群失调小鼠子宫内病原体负荷增加与中性粒细胞吞噬能力和反应性降低相关。因此，肠道菌群对S.通过调节SCFAs的水平和维持中性粒细胞的吞噬能力和应答性来治疗金黄色葡萄球菌诱导的子宫内膜炎。
Endometritis, the inflammation of the endometrial lining caused by bacterial pathogens, is associated with reproductive failure. Recent studies have shown that gut microbiota play an important role in infectious diseases. However, the roles of the gut microbiota in endometritis remain unclear. Here, we assessed the effects and mechanisms of the gut microbiota during endometritis induced byStaphylococcus aureus(S. aureus). A mouse gut microbiota-dysbiosis model was established by a mixture of antibiotics (Abx) and subsequently, a model of endometritis was established by the uterine perfusion ofS. aureus.Fecal microbiota transplantation (FMT) was performed to evaluate the relationship between gut microbiota and endometritis. The results showed that the mice with gut microbiota-dysbiosis developed uterine inflammation, while this inflammatory response of the uterus was alleviated in mice with FMT to gut microbiota-dysbiosis. In addition,S. aureus-induced endometritis was greater in severity in the mice with gut dysbiosis as compared to the untreated mice. Moreover, these effects were reversed in mice with FMT to the gut microbiota-dysbiosis. GC-MS analysis demonstrated that the levels of short-chain fatty acids (SCFAs) in the feces of mice with gut microbiota-dysbiosis significantly decreased and pretreatment with sodium butyrate or sodium propionate increased the concentrations of butyrate or propionate in both the circulation and uterine tissues, thereby reducing the severity of endometritis induced byS. aureus. In addition, the increased pathogen load in the uteri of the mice with gut microbiota-dysbiosis was associated with a reduction in the phagocytic ability and responsiveness of neutrophils. In conclusion, the gut microbiota offer a protective effect againstS. aureus-induced endometritis by regulating the levels of SCFAs and maintaining the phagocytic ability and responsiveness of neutrophils.