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首页> 外文期刊>Infection and immunity >The Posttranslocation Chaperone PrsA2 Contributes to Multiple Facets of Listeria monocytogenes Pathogenesis
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The Posttranslocation Chaperone PrsA2 Contributes to Multiple Facets of Listeria monocytogenes Pathogenesis

机译：易位伴侣蛋白PrsA2有助于单核细胞增多性李斯特菌发病机理的多个方面

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Listeria monocytogenes is an intracellular bacterial pathogen whose virulence depends on the regulated expression of numerous secreted bacterial factors. As for other gram-positive bacteria, many proteins secreted by L. monocytogenes are translocated across the bacterial membrane in an unfolded state to the compartment existing between the membrane and the cell wall. This compartment presents a challenging environment for protein folding due to its high density of negative charge, high concentrations of cations, and low pH. We recently identified PrsA2 as a gene product required for L. monocytogenes virulence. PrsA2 was identified based on its increased secretion by strains containing a mutationally activated form of prfA, the key regulator of L. monocytogenes virulence gene expression. The prsA2 gene product is one of at least two predicted peptidyl-prolyl cis/trans-isomerases encoded by L. monocytogenes; these proteins function as posttranslocation protein chaperones and/or foldases. In this study, we demonstrate that PrsA2 plays a unique and important role in L. monocytogenes pathogenesis by promoting the activity and stability of at least two critical secreted virulence factors: listeriolysin O (LLO) and a broad-specificity phospholipase. Loss of PrsA2 activity severely attenuated virulence in mice and impaired bacterial cell-to-cell spread in host cells. In contrast, mutants lacking prsA1 resembled wild-type bacteria with respect to intracellular growth and cell-to-cell spread as well as virulence in mice. PrsA2 is thus distinct from PrsA1 in its unique requirement for the stability and full activity of L. monocytogenes-secreted factors that contribute to host infection.
机译：单核细胞增生李斯特菌是一种细胞内细菌病原体，其毒性取决于许多分泌细菌因子的调控表达。至于其他革兰氏阳性细菌， L分泌许多蛋白质。单核细胞增生病以展开状态跨细菌膜转移到膜与细胞壁之间的隔室。该隔室由于其高密度的负电荷，高浓度的阳离子和低pH值，为蛋白质折叠提供了具有挑战性的环境。我们最近鉴定出PrsA2是 L所需的基因产物。单核细胞增生性毒力。根据含有 prfA （ L的关键调控因子）的突变激活形式的菌株增加的分泌来鉴定PrsA2。单核细胞增生毒力基因表达 prsA2 基因产物是 L编码的至少两个预测的肽基脯氨酰顺式 / 反式异构酶之一。单核细胞增生这些蛋白质起转位后蛋白质伴侣和/或折叠酶的作用。在这项研究中，我们证明PrsA2在 L中起着独特而重要的作用。促进至少两个关键的分泌性毒力因子：李斯特菌溶血素O（LLO）和广泛特异性磷脂酶的活性和稳定性，从而成为单核细胞增生病的发病机理。 PrsA2活性的丧失严重减弱了小鼠的毒力，并损害了宿主细胞中细菌细胞间的传播。相比之下，缺乏 prsA1 的突变体在小鼠细胞内生长，细胞间扩散以及毒力方面类似于野生型细菌。因此，PrsA2与PrsA1的区别在于对 L的稳定性和充分活性的独特要求。单核细胞增生因子分泌的因子导致宿主感染。

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