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Gut microbiota mediate the protective effects on endometritis induced by Staphylococcus aureus in mice.
Food & Function ( IF 5.1 ) Pub Date : 2020-04-02 , DOI: 10.1039/c9fo02963j
Xiaoyu Hu 1 , Ruiying Mu 2 , Mingyue Xu 1 , Xin Yuan 1 , Peng Jiang 1 , Jian Guo 1 , Yongguo Cao 1 , Naisheng Zhang 1 , Yunhe Fu 1
Affiliation  

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 by Staphylococcus 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 of S. 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 by S. 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 against S. aureus-induced endometritis by regulating the levels of SCFAs and maintaining the phagocytic ability and responsiveness of neutrophils.

中文翻译:

肠道菌群介导金黄色葡萄球菌对小鼠子宫内膜炎的保护作用。

子宫内膜炎是由细菌病原体引起的子宫内膜内膜炎症,与生殖衰竭有关。最近的研究表明,肠道菌群在传染病中起重要作用。然而,肠道菌群在子宫内膜炎中的作用仍不清楚。在这里,我们评估了金黄色葡萄球菌(金黄色葡萄球菌)引起的子宫内膜炎期间肠道菌群的作用和机制。通过抗生素(Abx)的混合物建立了小鼠肠道菌群失调模型,随后通过子宫内金黄色葡萄球菌的灌注建立了子宫内膜炎模型。进行粪便菌群移植(FMT)以评估肠道菌群与子宫内膜炎之间的关系。结果表明,肠道菌群失调的小鼠发生了子宫炎症,而FMT小鼠因肠道菌群失调而减轻了子宫的这种炎症反应。另外,与未治疗的小鼠相比,在肠道营养不良的小鼠中金黄色葡萄球菌引起的子宫内膜炎的严重程度更高。而且,这些作用在具有FMT的小鼠中被逆转为肠道菌群失调。GC-MS分析表明,肠道菌群失调症小鼠的粪便中的短链脂肪酸(SCFA)含量显着降低,丁酸钠或丙酸钠的预处理增加了循环和子宫中丁酸或丙酸的浓度。组织,从而降低了由金黄色葡萄球菌引起的子宫内膜炎的严重程度。此外,肠道微生物群失调症小鼠子宫中病原体负荷的增加与嗜中性白细胞的吞噬能力和反应性降低有关。总之,肠道菌群可通过调节SCFA的水平并维持嗜中性粒细胞的吞噬能力和反应性,对金黄色葡萄球菌引起的子宫内膜炎提供保护作用。
更新日期:2020-04-02
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