The Rumen Microbiota Contributes to the Development of Mastitis in Dairy Cows.
The Rumen Microbiota Contributes to the Development of Mastitis in Dairy Cows.
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DOI：
10.1128/spectrum.02512-21
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发表时间：
2022-02-23
影响因子：
3.7
通讯作者：
Fu Y
中科院分区：
文献类型：
--
作者：
Hu X;Li S;Mu R;Guo J;Zhao C;Cao Y;Zhang N;Fu Y
乳腺炎是奶牛的一种高度流行的疾病，通常由乳腺局部感染引起。我们以前的研究表明，肠道微生物群在小鼠乳腺炎的发展中起着重要作用。然而，瘤胃微生物区系对奶牛乳房炎的影响及其相关机制尚不清楚。本研究采用高精料喂养荷斯坦弗里斯兰奶牛8周，建立亚急性瘤胃酸中毒（SARA）模型，探讨瘤胃微生物区系对奶牛乳房炎的影响及其机制。然后，分析乳腺中的炎症反应以及瘤胃液、粪便和乳中的细菌群落。结果表明，SARA诱导乳腺炎症状，激活全身炎症反应，并增加血乳屏障，肠道屏障和瘤胃屏障的渗透性。进一步的研究表明，脂多糖（LPS），来自肠道的SARA奶牛，易位到血液中，并积累在乳腺。此外，SARA奶牛瘤胃中寡养单胞菌的丰度增加，泌乳小鼠经口给予寡养单胞菌引起乳腺炎。综上所述，我们的研究结果表明，乳腺炎是由外源性病原微生物以及内源性致病因素引起的。瘤胃内寡养单胞菌数量的增加和LPS从瘤胃向乳腺的转运是引起奶牛乳腺炎的重要内源性因素。我们的研究为靶向奶牛乳房炎瘤胃微生物群的新型治疗策略提供了基础。乳腺炎是人畜共患的常见病和多发病，尤其是在奶牛养殖业中，已造成巨大的经济损失，并带来有害物质残留、耐药菌等公共卫生风险。传统观点认为乳腺炎主要是由外源性病原菌感染乳腺引起的。我们的研究发现，乳腺炎的发生是由内源性途径引起的。有证据表明，瘤胃来源的LPS通过血液循环进入乳腺，破坏血-乳屏障，然后诱导奶牛乳腺炎症。此外，瘤胃中高丰度的寡养单胞菌与乳腺炎的发生密切相关。这项研究为利用瘤胃微生物群对抗奶牛乳房炎的新治疗策略提供了基础。
Mastitis, a highly prevalent disease in dairy cows, is commonly caused by local infection of the mammary gland. Our previous studies have suggested that the gut microbiota plays an important role in the development of mastitis in mice. However, the effects of rumen microbiota on bovine mastitis and the related mechanisms remain unclear. In this study, we assessed the effects and mechanisms of rumen microbiota on bovine mastitis based on the subacute rumen acidosis (SARA) model induced by feeding Holstein Frisian cows a high-concentrate diet for 8 weeks. Then, the inflammatory responses in the mammary gland and the bacterial communities of rumen fluid, feces, and milk were analyzed. The results showed that SARA induced mastitis symptoms in the mammary gland; activated a systemic inflammatory response; and increased the permeability of the blood-milk barrier, gut barrier, and rumen barrier. Further research showed that lipopolysaccharides (LPS), derived from the gut of SARA cows, translocated into the blood and accumulated in the mammary glands. Furthermore, the abundance of Stenotrophomonas was increased in the rumen of SARA cows, and mastitis was induced by oral administration of Stenotrophomonas in lactating mice. In conclusion, our findings suggested that mastitis is induced by exogenous pathogenic microorganisms as well as by endogenous pathogenic factors. Specifically, the elevated abundance of Stenotrophomonas in the rumen and LPS translocation from the rumen to the mammary gland were important endogenous factors that induced mastitis. Our study provides a foundation for novel therapeutic strategies that target the rumen microbiota in cow mastitis. IMPORTANCE Mastitis is a common and frequently occurring disease of humans and animals, especially in dairy farming, which has caused huge economic losses and brought harmful substance residues, drug-resistant bacteria, and other public health risks. The traditional viewpoint indicates that mastitis is mainly caused by exogenous pathogenic bacteria infecting the mammary gland. Our study found that the occurrence of mastitis was induced by the endogenous pathway. Evidence has shown that rumen-derived LPS enters the mammary gland through blood circulation, damaging the blood-milk barrier and then inducing inflammation of the mammary gland in cows. In addition, a higher abundance of Stenotrophomonas in the rumen was closely associated with the development of mastitis. This study provides a basis for novel therapeutic strategies that exploit the rumen microbiota against mastitis in cows.
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DOI：
10.1292/jvms.17-0710
发表时间：
2018-06-29
期刊：
The Journal of veterinary medical science
影响因子：
--
作者：
Kurumisawa T;Kano R;Nakamura Y;Hibana M;Ito T;Kamata H;Suzuki K
通讯作者：
Suzuki K
影响因子：
3.5
作者：
Coon, R. E.;Duffield, T. F.;DeVries, T. J.
通讯作者：
DeVries, T. J.
DOI：
10.3923/pjbs.2013.1653.1661
发表时间：
2013-12-01
期刊：
Pakistan journal of biological sciences : PJBS
影响因子：
--
作者：
Deb, Rajib;Kumar, Amit;Kumar, Sushil
通讯作者：
Kumar, Sushil
影响因子：
3.7
作者：
Kobayashi K;Oyama S;Numata A;Rahman MM;Kumura H
通讯作者：
Kumura H
饲喂高谷物饮食可降低山羊肝脏中 LPS 清除率并增强免疫基因表达
影响因子：
2.6
作者：
Chang G;Zhang K;Xu T;Jin D;Seyfert HM;Shen X;Zhuang S
通讯作者：
Zhuang S