...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >Gas6 negatively regulates the Staphylococcus aureus-induced inflammatory response via TLR signaling in the mouse mammary gland
【24h】

Gas6 negatively regulates the Staphylococcus aureus-induced inflammatory response via TLR signaling in the mouse mammary gland

机译：Gas6负调节的葡萄球菌通过TLR aureus-induced炎症反应信号在鼠标乳腺

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Staphylococcus aureus (S. aureus)-induced mastitis is the most frequent, pathogenic, and prevalent infection of the mammary gland. The ligand growth arrest-specific 6 (Gas6) is a secretory protein that binds to and activates Tyro3, Axl, and MerTK receptors. This study explored the role of Gas6 in S. aureus-induced mastitis. Our results revealed that TLR receptors initiate the innate immune response in mammary gland tissues and epithelial cells and that introducing S. aureus activates TLR2 and TLR6 to drive multiple intracellular mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-kB) pathways. Moreover, S. aureus also induces Gas6, which then activates the TAM receptor kinase pathway, which is related to the inhibition of TLR2- and TLR6-mediated inflammatory pathways through SOCS1 and SOCS3 induction. Gas6 absence alone was found to be involved in the down-regulation of TAM receptor-mediated anti-inflammatory effects by inducing significantly prominent expression of TRAF6 and low protein and messenger RNA expression of SOCS1 and SOCS3. S. aureus-induced MAPK and NF-kB p65 phos-phorylation were also dependent on Gas6, which negatively regulated the production of Pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in S. aureus-treated mammary tissues and mammary epithelial cells. Our in vivo and in vitro study uncovered the Gas6-mediated negative feedback mechanism, which inhibits TLR2- and TLR6-mediated MAPK and NF-kB signaling by activating TAM receptor kinase (MerTK, Axl, and Tyro3) through the induction of SOCS1/SOCS3 proteins.
机译：金黄色葡萄球菌(金黄色葡萄球菌)全身的乳腺炎是最常见的病原,流行吗乳腺的感染。arrest-specific 6 (Gas6)是一种分泌蛋白结合并激活Tyro3,妳,MerTK受体。在美国aureus-induced乳腺炎。透露,toll样受体启动先天乳腺组织和免疫反应上皮细胞,介绍金黄色葡萄球菌激活TLR2和TLR6驱动多个细胞内增殖蛋白激酶(MAPK)和核转录因子kappa-B (NF-kB)通路。然后TAM受体激酶激活通路,从而抑制有关TLR2, TLR6-mediated炎症通路通过SOCS1 SOCS3归纳。被发现参与下调TAM受体介导的抗炎作用的诱导表达式TRAF6和显著突出低蛋白质和SOCS1的信使RNA表达和SOCS3。phos-phorylation也依赖Gas6,负调控生产促炎细胞因子(il - 1β,il - 6,肿瘤坏死因子-α)在美国aureus-treated乳腺组织和乳腺上皮细胞。体外研究发现Gas6-mediated负面的抑制TLR2和反馈机制TLR6-mediated MAPK和NF-kB信号激活TAM受体激酶(MerTK,妳通过感应SOCS1 / SOCS3 Tyro3)蛋白质。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号