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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Negative regulation of Salmonella pathogenicity island 2 is required for contextual control of virulence during typhoid
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Negative regulation of Salmonella pathogenicity island 2 is required for contextual control of virulence during typhoid

机译：沙门氏菌致病岛2的负调控是伤寒期间毒力的上下文控制所必需的

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摘要

Salmonella enterica relies on a type III secretion system encoded in Salmonella pathogenicity island-2 (SPI-2) to survive and replicate within macrophages at systemic sites during typhoid. SPI-2 virulence is induced upon entry into macrophages, but the mechanisms of SPI-2 gene control in vivo remain unclear, particularly with regard to negative regulators that control the contextual activation of SPI-2. Here, we identified and characterized YdgT as a negative modulator of the SPI-2 pathogenicity island and established that this negative regulation is central to systemic pathogenesis because ydgT mutants overexpressing typhoid virulence genes were ultimately attenuated during infection. ydgT mutants displayed a biphasic virulence phenotype during in vivo competitive infections that consisted of an early "gain-of-virulence" dependent on SPI-2 activation, followed by attenuation later in infection indicating that proper contextual regulation of SPI-2 by YdgT is necessary for full virulence during systemic colonization. These data suggest that overexpression of virulence-associated type III secretion genes can have an adverse effect on bacterial pathogenesis in vivo.
机译：肠伤寒沙门氏菌依靠伤寒沙门氏菌致病岛2（SPI-2）中编码的III型分泌系统在伤寒过程中在系统位点的巨噬细胞中生存和复制。进入巨噬细胞时会诱导SPI-2毒力，但体内SPI-2基因控制的机制仍不清楚，尤其是对于控制SPI-2的背景活化的负调节剂而言。在这里，我们将YdgT鉴定为SPI-2致病岛的负调节剂，并确定该负调节是系统发病机制的关键，因为过表达伤寒毒力基因的ydgT突变体在感染过程中最终被减弱。 ydgT突变体在体内竞争性感染过程中表现出双相毒力表型，包括依赖于SPI-2激活的早期“毒力获得”，随后在感染中减弱，表明通过YdgT对SPI-2进行适当的环境调节是必要的在系统定植期间具有完全的毒性。这些数据表明，与毒性相关的III型分泌基因的过度表达可能对体内细菌发病机理产生不利影响。

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