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肠道微生物群有助于金黄色葡萄球菌诱导的小鼠乳腺炎的发展。

The gut microbiota contributes to the development of Staphylococcus aureus-induced mastitis in mice.

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062, Jilin, People's Republic of China.

出版信息

ISME J. 2020 Jul;14(7):1897-1910. doi: 10.1038/s41396-020-0651-1. Epub 2020 Apr 27.

Abstract

Mastitis is one of the most prevalent diseases in dairy farming worldwide. The gut microbiota plays an important role in the regulation of systemic and local inflammatory diseases, such as mastitis. However, the regulatory mechanism of the gut microbiota on mastitis is still unclear. Thus, the aim of this study was to investigate the function and regulatory mechanisms of the gut microbiota in host defense against mastitis caused by Staphylococcus aureus (S. aureus) infection. Increased blood-milk barrier permeability, and S. aureus-induced mastitis severity were observed gut microbiota-dysbiosis mice compared with those in control mice. Moreover, feces microbiota transplantation (FMT) to microbbiota-dysbiosis mice reversed these effects. Furthermore, established disruption of commensal homeostasis results in significantly increased abundance of pathogenic Enterobacter bacteria, while the relative abundance of short-chain fatty acid (SCFAs)-producing bacterial phyla (Firmicutes and Bacteroidetes) was significantly reduced. However, FMT to gut microbiota-dysbiosis mice reversed these changes. In addition, dysbiosis reduced the levels of SCFAs, and administration of sodium propionate, sodium butyrate, and probiotics (butyrate-producing bacteria) reversed the changes in the blood-milk barrier and reduced the severity of mastitis induced by S. aureus. In conclusion, this new finding demonstrated that the gut microbiota acts as a protective factor in host defense against mastitis and that targeting the gut-mammary gland axis represents a promising therapeutic approach for mastitis treatment.

摘要

乳腺炎是全球奶牛养殖业中最常见的疾病之一。肠道微生物群在调节全身和局部炎症性疾病(如乳腺炎)方面发挥着重要作用。然而,肠道微生物群对乳腺炎的调节机制尚不清楚。因此,本研究旨在探讨肠道微生物群在宿主防御金黄色葡萄球菌(S. aureus)感染引起的乳腺炎中的功能和调节机制。与对照组小鼠相比,肠道微生物群失调小鼠表现出血液-乳汁屏障通透性增加和金黄色葡萄球菌诱导的乳腺炎严重程度增加。此外,肠道微生物群失调小鼠的粪便微生物群移植(FMT)逆转了这些效应。此外,定植菌稳态的破坏显著增加了致病性肠杆菌的丰度,而短链脂肪酸(SCFA)产生菌门(厚壁菌门和拟杆菌门)的相对丰度显著降低。然而,FMT 到肠道微生物群失调小鼠逆转了这些变化。此外,失调降低了 SCFA 的水平,而丙酸钠、丁酸钠和益生菌(产生丁酸的细菌)的给药逆转了血液-乳汁屏障的变化,并减轻了金黄色葡萄球菌诱导的乳腺炎的严重程度。总之,这一新发现表明肠道微生物群在宿主防御乳腺炎中起保护作用,靶向肠道-乳腺轴可能代表一种有前途的乳腺炎治疗方法。

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