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首页> 外文期刊>Infection and immunity >Arginine-143 of Yersinia enterocolitica YopP Crucially Determines Isotype-Related NF-κB Suppression and Apoptosis Induction in Macrophages
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Arginine-143 of Yersinia enterocolitica YopP Crucially Determines Isotype-Related NF-κB Suppression and Apoptosis Induction in Macrophages

机译：小肠结肠炎耶尔森氏菌YopP的精氨酸143至关重要地确定同型相关的NF-κB抑制和巨噬细胞凋亡的诱导。

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Pathogenic Yersinia spp. counteract host defense mechanisms by modulating the cellular signal relay in response to infection. Subversion of the antiapoptotic NF-κB signaling pathway by the Yersinia enterocolitica virulence protein YopP crucially determines the induction of apoptosis inYersinia-infected macrophages. Here, we analyzed a panel of pathogenic, phylogenetically distinct Y. enterocolitica serotypes for their abilities to trigger macrophage apoptosis. Y. enterocolitica from the highly pathogenic serogroup O8 was substantially more effective in apoptosis induction than Yersinia from the serogroups O3 and O9. Complementation of yopP-knockout mutants revealed that this effect was specifically conferred by the serogroup O8 YopP. The amino acid sequences of YopPO8 and YopPO9 share 94% identity, and both YopP isotypes were found to interact with the NF-κB-activating kinase IKKβ in macrophages. However, selectively, YopPO8 mediated efficient inhibition of IKKβ activities, which led to substantial suppression of NF-κB activation. To localize the YopPO8-related effector domain, we interchanged stretches of amino acids and single amino acid residues between YopPO8 and YopPO9. Functional characterization of the resulting mutants revealed a major role of the arginine-143 residue in determining the inhibitory impact of YopP on IKKβ activity and survival of macrophages.
机译：致病性耶尔森氏菌 spp。通过响应感染而调节细胞信号中继来对抗宿主防御机制。小肠结肠炎耶尔森氏菌毒性蛋白YopP颠覆抗凋亡的NF-κB信号通路至关重要地决定了感染小肠结肠炎耶尔森氏菌的巨噬细胞的凋亡诱导。在这里，我们分析了一组致病的，系统发育上独特的 Y。肠结肠炎血清型触发巨噬细胞凋亡的能力。是的高致病性血清型O8的肠结肠炎比O3和O9血清型的<耶尔森菌更有效。补充 yopP -敲除突变体表明，这种作用是由血清型O8 YopP专门赋予的。 YopPO8和YopPO9的氨基酸序列具有94％的同一性，并且发现两种YopP同种型均与巨噬细胞中的NF-κB激活激酶IKKβ相互作用。然而，选择性地，YopPO8介导了对IKKβ活性的有效抑制，从而导致了NF-κB激活的显着抑制。为了定位YopPO8相关的效应子域，我们在YopPO8和YopPO9之间交换了一段氨基酸和单个氨基酸残基。所得突变体的功能表征揭示了精氨酸143残基在确定YopP对IKKβ活性和巨噬细胞存活的抑制作用中的主要作用。

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