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首页> 外文期刊>Infection and immunity >Growth of Yersinia pseudotuberculosis in Mice Occurs Independently of Toll-Like Receptor 2 Expression and Induction of Interleukin-10
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Growth of Yersinia pseudotuberculosis in Mice Occurs Independently of Toll-Like Receptor 2 Expression and Induction of Interleukin-10

机译：小鼠耶尔森氏菌假结核的生长独立于Toll样受体2的表达和白介素10的诱导

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摘要

Pathogenic Yersinia translocates effector proteins into target cells via a type III secretion system (TTSS), modulating the host immune response. A component of the TTSS translocon, LcrV, has been implicated in preventing inflammation through Toll-like receptor 2 (TLR2) by inducing expression of the anti-inflammatory cytokine interleukin-10 (IL-10). TLR2?/? mice were reported to be less susceptible to the enteropathogen Yersinia enterocolitica. To determine whether TLR2 also plays a role in recognition of the enteropathogen Yersinia pseudotuberculosis and whether this results in an immune response that is detrimental to the host, we evaluated the macrophage cytokine response to live Y. pseudotuberculosis and analyzed the susceptibility of TLR2?/? mice to enteropathogenic Yersinia. We find that Yersinia induction of macrophage IL-10 occurs independently of TLR2 and LcrV and is blocked by the TTSS. In particular, the TTSS effector protein YopJ, which inhibits production of the inflammatory cytokine tumor necrosis factor alpha (TNF-α), also inhibits IL-10 expression. Consistent with these results, IL-10 is undetectable in Y. pseudotuberculosis-infected mouse tissues until advanced stages of infection. In addition, we find that TLR2?/? mice (derived independently from those used in previous studies) do not display altered susceptibility to enteropathogenic Yersinia compared to wild-type mice. Tissue levels of IL-10, as well as the inflammatory cytokines TNF-α, IL-6, and gamma interferon and the chemokine macrophage chemotactic protein 1, are similar in TLR2+/+ and TLR2?/? mice during enteropathogenic Yersinia infection. Therefore, the absence of TLR2 alone does not affect the cytokine response of macrophages to, or the in vivo growth and survival of, enteropathogenic Yersinia.
机译：致病性耶尔森氏菌通过III型分泌系统（TTSS）将效应蛋白转运到靶细胞中，从而调节宿主的免疫反应。 TTSS转运蛋白的一个组成部分LcrV与通过诱导抗炎细胞因子白介素10（IL-10）的表达通过Toll样受体2（TLR2）预防炎症有关。据报道，TLR2 ？/？小鼠对肠病原体小肠结肠炎耶尔森氏菌的敏感性较低。为了确定TLR2是否也在识别肠病原耶尔森氏菌假结核中发挥作用，以及这是否导致对宿主有害的免疫应答，我们评估了巨噬细胞对活体 Y的细胞因子应答。假结核并分析了TLR2 ？/？小鼠对肠致病性耶尔森氏菌的敏感性。我们发现巨噬细胞IL-10的耶尔森氏菌诱导独立于TLR2和LcrV发生，并被TTSS阻断。特别地，抑制炎症性细胞因子肿瘤坏死因子α（TNF-α）产生的TTSS效应蛋白YopJ也抑制IL-10表达。与这些结果一致，在 Y中未检测到IL-10。感染假结核病的小鼠组织，直至感染晚期。此外，我们发现与野生型小鼠相比，TLR2 ？/？小鼠（独立于先前研究中的小鼠）对肠道致病性耶尔森菌的易感性没有改变。在TLR2 + / + 和TLR2 ？/？小鼠在肠道致病性耶尔森氏菌感染期间。因此，单独缺乏TLR2不会影响巨噬细胞对肠致病性耶尔森氏菌的细胞因子应答或体内生长和存活。

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