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首页> 外文期刊>Infection and immunity >IscR Is a Global Regulator Essential for Pathogenesis of Vibrio vulnificus and Induced by Host Cells
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IscR Is a Global Regulator Essential for Pathogenesis of Vibrio vulnificus and Induced by Host Cells

机译：IscR是弧菌弧菌的发病机理和由宿主细胞诱导的全球必需调节剂。

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A mutant that exhibited less cytotoxic activity toward INT-407 human intestinal epithelial cells than the wild type was screened from a random transposon mutant library of Vibrio vulnificus, and an open reading frame encoding an Fe-S cluster regulator, IscR, was identified using a transposon-tagging method. A mutational analysis demonstrated that IscR contributes to mouse mortality as well as cytotoxicity toward the INT-407 cells, indicating that IscR is essential for the pathogenesis of V. vulnificus. A whole-genome microarray analysis revealed that IscR influenced the expression of 67 genes, of which 52 were upregulated and 15 were downregulated. Among these, 12 genes most likely involved in motility and adhesion to host cells, hemolytic activity, and survival under oxidative stress of the pathogen during infection were selected and experimentally verified to be upregulated by IscR. Accordingly, the disruption of iscR resulted in a significant reduction in motility and adhesion to INT-407 cells, in hemolytic activity, and in resistance to reactive oxygen species (ROS) such as H2O2 and tert-butyl hydroperoxide (t-BOOH). Furthermore, the present study demonstrated that iscR expression was induced by exposure of V. vulnificus to the INT-407 cells, and the induction appeared to be mediated by ROS generated by the host cells during infection. Consequently, the combined results indicated that IscR is a global regulator that contributes to the overall success in the pathogenesis of V. vulnificus by regulating the expression of various virulence and survival genes in addition to Fe-S cluster genes.
机译：从野生弧菌的转座子突变体文库中筛选出了比野生型对INT-407人肠道上皮细胞具有更少细胞毒活性的突变体，并使用A.S.R鉴定了编码Fe-S簇调节剂IscR的开放阅读框。转座子标记法。突变分析表明，IscR导致小鼠死亡以及对INT-407细胞的细胞毒性，表明IscR对于创伤弧菌的发病机理至关重要。全基因组微阵列分析表明，IscR影响了67个基因的表达，其中52个基因上调，而15个基因下调。在这些基因中，选择了12个最有可能与感染过程中病原体的运动性和粘附性，溶血活性和病原体在氧化应激下的存活有关的12个基因，并通过实验验证了它们被IscR上调。因此， iscR 的破坏导致运动性和对INT-407细胞的粘附，溶血活性以及对活性氧（ROS）如H 2 < / sub> O 2 和叔-丁基氢过氧化物（ t -BOOH）。此外，本研究证明 iscR 表达是通过将创伤弧菌暴露于INT-407细胞而诱导的，并且诱导似乎是由宿主细胞在感染过程中产生的ROS介导的。因此，综合结果表明，IscR是一种全局调节剂，通过调节除Fe-S簇基因之外的各种毒力和存活基因的表达，有助于创伤弧菌的整体成功。

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