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假结核耶尔森菌效应蛋白YopH和YopE在肠道和淋巴组织定殖及持续存在中的需求

Requirement of the Yersinia pseudotuberculosis effectors YopH and YopE in colonization and persistence in intestinal and lymph tissues.

作者信息

Logsdon Lauren K, Mecsas Joan

机构信息

Department of Microbiology and Molecular Biology, Tufts University, Boston, Massachusetts 02111, USA.

出版信息

Infect Immun. 2003 Aug;71(8):4595-607. doi: 10.1128/IAI.71.8.4595-4607.2003.

DOI:10.1128/IAI.71.8.4595-4607.2003
PMID:12874339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC166012/
Abstract

The gram-negative enteric pathogen Yersinia pseudotuberculosis employs a type III secretion system and effector Yop proteins that are required for virulence. Mutations in the type III secretion-translocation apparatus have been shown to cause defects in colonization of the murine cecum, suggesting roles for one or more effector Yops in the intestinal tract. To investigate this possibility, isogenic yop mutant strains were tested for their ability to colonize and persist in intestinal and associated lymph tissues of the mouse following orogastric inoculation. In single-strain infections, a yopHEMOJ mutant strain was unable to colonize, replicate, or persist in intestinal and lymph tissues. A yopH mutant strain specifically fails to colonize the mesenteric lymph nodes, but yopE and yopO mutant strains showed only minor defects in persistence in intestinal and lymph tissues. While no single Yop was found to be essential for colonization or persistence in intestinal tissues in single-strain infections, the absence of both YopH and YopE together almost eliminated colonization of all tissues, indicating either that these two Yops have some redundant functions or that Y. pseudotuberculosis employs multiple strategies for colonization. In competition infections with wild-type Y. pseudotuberculosis, the presence of wild-type bacteria severely hindered the ability of the yopH, yopE, and yopO mutants to persist in many tissues, suggesting that the wild-type bacteria either fills colonization niches or elicits host responses that the yop mutants are unable to withstand.

摘要

革兰氏阴性肠道病原体假结核耶尔森菌利用三型分泌系统和效应子Yop蛋白,这些对于其毒力是必需的。已证明三型分泌-转运装置中的突变会导致小鼠盲肠定殖缺陷,这表明一种或多种效应子Yop在肠道中发挥作用。为了研究这种可能性,对同基因的yop突变株进行了测试,以检测它们在经口胃接种后在小鼠肠道及相关淋巴组织中定殖和持续存在的能力。在单菌株感染中,yopHEMOJ突变株无法在肠道和淋巴组织中定殖、复制或持续存在。yopH突变株特别无法定殖于肠系膜淋巴结,但yopE和yopO突变株在肠道和淋巴组织中的持续存在仅表现出轻微缺陷。虽然在单菌株感染中未发现单一的Yop对于肠道组织的定殖或持续存在是必不可少的,但同时缺失YopH和YopE几乎消除了所有组织的定殖,这表明这两种Yop具有一些冗余功能,或者假结核耶尔森菌采用多种定殖策略。在与野生型假结核耶尔森菌的竞争感染中,野生型细菌的存在严重阻碍了yopH、yopE和yopO突变株在许多组织中持续存在的能力,这表明野生型细菌要么占据定殖位点,要么引发yop突变株无法抵御的宿主反应。

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本文引用的文献

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The virulence protein Yop5 of Yersinia pseudotuberculosis is regulated at transcriptional level by plasmid-plB1 -encoded trans-acting elements controlled by temperature and calcium.假结核耶尔森菌的毒力蛋白Yop5在转录水平上受质粒pIB1编码的、受温度和钙调控的反式作用元件的调控。
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The yersinia virulence factor YopM forms a novel protein complex with two cellular kinases.耶尔森氏菌毒力因子YopM与两种细胞激酶形成一种新型蛋白质复合物。
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YopH prevents monocyte chemoattractant protein 1 expression in macrophages and T-cell proliferation through inactivation of the phosphatidylinositol 3-kinase pathway.YopH 通过使磷脂酰肌醇 3-激酶途径失活,来阻止巨噬细胞中单核细胞趋化蛋白 1 的表达以及 T 细胞增殖。
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EspG, a novel type III system-secreted protein from enteropathogenic Escherichia coli with similarities to VirA of Shigella flexneri.EspG,一种来自肠致病性大肠杆菌的新型III型系统分泌蛋白,与福氏志贺菌的VirA相似。
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YopB of Yersinia enterocolitica is essential for YopE translocation.小肠结肠炎耶尔森菌的YopB对于YopE的转运至关重要。
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