TLR2 信号通路通过诱导线粒体活性氧产生来抵抗感染。

TLR2 Signaling Pathway Combats Infection by Inducing Mitochondrial Reactive Oxygen Species Production.

机构信息

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

Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai 200241, China.

出版信息

Cells. 2020 Feb 21;9(2):494. doi: 10.3390/cells9020494.

Mastitis caused by () is a common and difficult-to-cure clinical disease in dairy cows. In this study, the role of Toll-like receptors (TLRs) and TLR-mediated signaling pathways in mastitis caused by was investigated using mouse models and mammary epithelial cells (MECs). We used to infect mammary glands of wild type, TLR2 and TLR4 mice and quantified the adaptor molecules in TLR signaling pathways, proinflammatory cytokines, tissue damage, and bacterial count. When compared with TLR4 deficiency, TLR2 deficiency induced more severe pathological changes through myeloid differentiation primary response 88 (MyD88)-mediated signaling pathways during infection. In MECs, TLR2 detected infection and induced mitochondrial reactive oxygen species (mROS) to assist host in controlling the secretion of inflammatory factors and the elimination of intracellular . Our results demonstrated that TLR2-mediated mROS has a significant effect on -induced host defense responses in mammary glands as well as in MECs.

由引起的乳腺炎是奶牛中一种常见且难以治愈的临床疾病。在这项研究中，使用小鼠模型和乳腺上皮细胞（MEC）研究了 Toll 样受体（TLR）和 TLR 介导的信号通路在由引起的乳腺炎中的作用。我们使用感染野生型、TLR2 和 TLR4 小鼠的乳腺，并定量分析 TLR 信号通路中的衔接分子、促炎细胞因子、组织损伤和细菌计数。与 TLR4 缺陷相比，TLR2 缺陷通过髓样分化初级反应 88（MyD88）介导的信号通路在感染时引起更严重的病理变化。在 MEC 中，TLR2 检测到感染，并诱导线粒体活性氧（mROS）以协助宿主控制炎症因子的分泌和细胞内的清除。我们的结果表明，TLR2 介导的 mROS 对诱导的乳腺宿主防御反应以及 MEC 具有重要作用。