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首页> 外文期刊>Infection and immunity >Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium
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Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium

机译：VI型分泌系统相关的基因簇有助于肠炎沙门氏菌鼠伤寒沙门氏菌的发病机理。

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The enteropathogen Salmonella enterica serovar Typhimurium employs a suite of tightly regulated virulence factors within the intracellular compartment of phagocytic host cells resulting in systemic dissemination in mice. A type VI secretion system (T6SS) within Salmonella pathogenicity island 6 (SPI-6) has been implicated in this process; however, the regulatory inputs and the roles of noncore genes in this system are not well understood. Here we describe four clusters of noncore T6SS genes in SPI-6 based on a comparative relationship with the T6SS-3 of Burkholderia mallei and report that the disruption of these genes results in defects in intracellular replication and systemic dissemination in mice. In addition, we show that the expression of the SPI-6-encoded Hcp and VgrG orthologs is enhanced during late stages of macrophage infection. We identify six regions that are transcriptionally active during cell infections and that have regulatory contributions from the regulators of virulence SsrB, PhoP, and SlyA. We show that levels of protein expression are very weak under in vitro conditions and that expression is not enhanced upon the deletion of ssrB, phoP, slyA, qseC, ompR, or hfq, suggesting an unknown activating factor. These data suggest that the SPI-6 T6SS has been integrated into the Salmonella Typhimurium virulence network and customized for host-pathogen interactions through the action of noncore genes.
机译：肠病原肠小肠沙门氏菌鼠伤寒沙门氏菌在吞噬性宿主细胞的细胞内区室中使用了一组严格调节的致病因子，可导致小鼠全身传播。该过程涉及沙门氏菌致病岛6（SPI-6）中的VI型分泌系统（T6SS）。然而，对该系统的调控输入和非核心基因的作用尚不十分了解。在这里，我们根据与Burkholderia mallei的T6SS-3的比较关系，描述了SPI-6中的四个非核心T6SS基因簇，并报告了这些基因的破坏导致小鼠细胞内复制和系统性传播的缺陷。此外，我们表明在巨噬细胞感染的后期，SPI-6编码的Hcp和VgrG直向同源物的表达增强。我们确定了六个区域在细胞感染过程中具有转录活性，并具有来自毒力SsrB，PhoP和SlyA调节因子的调节作用。我们显示蛋白质表达水平在体外条件下非常弱，并且在删除 ssrB ， phoP ，< em> slyA ， qseC ， ompR 或 hfq ，提示激活因子未知。这些数据表明，SPI-6 T6SS已整合到鼠伤寒沙门氏菌毒力网络中，并通过非核心基因的作用针对宿主-病原体相互作用进行了定制。

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