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首页> 外文期刊>Infection and immunity >Modulation of Virulence by Two Acidified Nitrite-Responsive Loci of Salmonella enterica Serovar Typhimurium
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Modulation of Virulence by Two Acidified Nitrite-Responsive Loci of Salmonella enterica Serovar Typhimurium

机译：肠炎沙门氏菌血清型鼠伤寒沙门氏菌的两个酸化亚硝酸盐响应基因座对毒力的调节。

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Two acidified nitrite-inducible genes of Salmonella enterica serovar Typhimurium were identified with a green fluorescent protein-based promoter-trap screen. The nitrite-inducible promoters were located upstream of loci that we designated nipAB and nipC, which correspond to hcp-hcr (hybrid cluster protein) of Escherichia coli and norA of Alcaligenes eutrophus, respectively. Maximal induction of the promoters by nitrite was dependent on pH. The nipAB promoter was regulated by oxygen in an Fnr-dependent manner. The nipC promoter was also regulated by oxygen but in an Fnr-independent manner. The promoters were upregulated in activated RAW264.7 macrophage-like cells, which produce NO via the inducible nitric oxide synthase (iNOS), and the induction was inhibited by aminoguanidine, an inhibitor of iNOS. Although the nipAB and nipC mutants displayed no defects under a variety of in vitro conditions or in tissue culture infections, they exhibited lower oral 50% lethal doses (LD50s) than did the wild type in C57BL/6J mouse infections. The lower LD50s reflected an unexpected increased ability of small inoculating doses of the mutant bacteria to cause lethal infection 2 to 3 weeks after challenge, compared to a similar challenge dose of wild-type bacteria. We conclude that these genes are regulated by physiological nitrogen oxides and that the absence of these bacterial genes in some way diminishes the ability of mice to clear a low dose infection.
机译：通过基于绿色荧光蛋白的启动子-诱捕筛选，鉴定了两个沙门氏菌鼠伤寒沙门氏菌的酸化亚硝酸盐诱导基因。亚硝酸盐诱导型启动子位于我们命名为 nipAB 和 nipC 的基因座的上游，它们分别对应于 hcp-hcr （杂交簇蛋白）嗜碱性产碱杆菌的大肠杆菌和 norA 。亚硝酸盐对启动子的最大诱导取决于pH。 nipAB 启动子受氧气以Fnr依赖性方式调节。 nipC 启动子也受到氧气的调节，但与Fnr无关。启动子在活化的RAW264.7巨噬细胞样细胞中被上调，该细胞通过诱导型一氧化氮合酶（iNOS）产生NO，并且诱导被iNOS的抑制剂氨基胍抑制。尽管 nipAB 和 nipC 突变体在多种体外条件下或在组织培养感染中均未显示缺陷，但它们的口服50％致死剂量较低（LD 50 s）比C57BL / 6J小鼠感染中的野生型好。较低的LD 50 反映了与类似剂量的野生型细菌相比，小剂量接种的突变细菌在攻击后2至3周引起致命感染的能力意外增强。我们得出的结论是，这些基因受生理性氮氧化物的调节，而这些细菌基因的缺失会以某种方式减弱小鼠清除低剂量感染的能力。

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