Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People Republic of China.
Linqu Animal Husbandry Bureau, China.
Food Funct. 2020 Apr 30;11(4):3695-3705. doi: 10.1039/c9fo02963j.
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.
子宫内膜炎是由细菌病原体引起的子宫内膜炎症，与生殖失败有关。最近的研究表明，肠道微生物群在传染病中发挥着重要作用。然而，肠道微生物群在子宫内膜炎中的作用尚不清楚。在这里，我们评估了肠道微生物群在金黄色葡萄球菌（S. aureus）引起的子宫内膜炎中的作用和机制。通过抗生素（Abx）混合物建立了一种小鼠肠道微生物群失调模型，随后通过子宫内灌注金黄色葡萄球菌建立了子宫内膜炎模型。进行粪便微生物群移植（FMT）以评估肠道微生物群与子宫内膜炎之间的关系。结果表明，肠道微生物群失调的小鼠发生了子宫炎症，而 FMT 到肠道微生物群失调的小鼠的子宫炎症反应得到了缓解。此外，与未处理的小鼠相比，肠道失调的小鼠金黄色葡萄球菌引起的子宫内膜炎更为严重。此外，FMT 到肠道微生物群失调的小鼠中这些作用得到了逆转。GC-MS 分析表明，肠道微生物群失调小鼠粪便中的短链脂肪酸（SCFAs）水平显著降低，而用丁酸钠或丙酸钠预处理可增加循环和子宫组织中丁酸盐或丙酸盐的浓度，从而减轻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有关。总之，肠道微生物群通过调节 SCFAs 水平并维持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。
