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牛磺酸通过降低 ROS-HIF1α 驱动的糖酵解缓解感染。

Reduction of ROS-HIF1α-driven glycolysis by taurine alleviates infection.

机构信息

MOE Joint International Research Laboratory of Animal Health and Food Safety, Key Laboratory of Animal Physiology & Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.

National Research Center for Veterinary Vaccine Engineering and Technology of China, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China.

出版信息

Food Funct. 2022 Feb 21;13(4):1774-1784. doi: 10.1039/d1fo03909a.

DOI:10.1039/d1fo03909a
PMID:35112684
Abstract

Antibiotic-resistant strains of () frequently cause clinical mastitis in dairy cows resulting in enormous economic losses. The regulation of immunometabolism is a promising strategy for controlling this bacterial infection. To investigate whether taurine alleviates infection by the regulation of host glycolysis HIF1α, the murine mammary epithelial cell line (EpH4-Ev) and C57BL/6J mice were challenged with Our data indicate that HIF1α-driven glycolysis promotes inflammation and damage in response to the challenge. The activation of HIF1α is dependent on mTOR-mediated ROS production. These results were confirmed . Taurine, an intracellular metabolite present in most animal tissues, has been shown to effectively modulate HIF1α-triggered metabolic reprogramming and contributes to a reduction of inflammation, which reduces mammary tissue damage and prevents mammary gland dysfunction in -induced mastitis. These data provide a novel putative prophylactic and therapeutic strategy for amelioration of dairy cow mastitis and bacterial inflammation.

摘要

(金黄色葡萄球菌)耐药菌株常导致奶牛临床乳腺炎,造成巨大的经济损失。免疫代谢调控是控制这种细菌感染的一种有前途的策略。为了研究牛磺酸是否通过调节宿主糖酵解 HIF1α来缓解金黄色葡萄球菌感染,本研究用金黄色葡萄球菌()感染小鼠乳腺上皮细胞系(EpH4-Ev)和 C57BL/6J 小鼠。我们的数据表明,HIF1α 驱动的糖酵解促进了炎症和损伤对金黄色葡萄球菌的反应。HIF1α 的激活依赖于 mTOR 介导的 ROS 产生。这些结果得到了进一步的证实。牛磺酸是一种存在于大多数动物组织中的细胞内代谢物,已被证明能有效地调节 HIF1α 触发的代谢重编程,并有助于减少炎症,从而减轻乳腺炎引起的乳腺组织损伤和防止乳腺功能障碍。这些数据为改善奶牛乳腺炎和细菌炎症提供了一种新的有前途的预防和治疗策略。

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Food Funct. 2022 Feb 21;13(4):1774-1784. doi: 10.1039/d1fo03909a.
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