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首页> 外文期刊>Infection and immunity >CsrA and Cra Influence Shigella flexneri Pathogenesis
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CsrA and Cra Influence Shigella flexneri Pathogenesis

机译：CsrA和Cra影响弗氏志贺氏菌发病机理

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Shigella flexneri is a facultative intracellular pathogen that invades and disrupts the colonic epithelium. In order to thrive in the host, S. flexneri must adapt to environmental conditions in the gut and within the eukaryotic cytosol, including variability in the available carbon sources and other nutrients. We examined the roles of the carbon consumption regulators CsrA and Cra in a cell culture model of S. flexneri virulence. CsrA is an activator of glycolysis and a repressor of gluconeogenesis, and a csrA mutant had decreased attachment and invasion of cultured cells. Conversely, Cra represses glycolysis and activates gluconeogenesis, and the cra mutant had an increase in both attachment and invasion compared to the wild-type strain. Both mutants were defective in plaque formation. The importance of the glycolytic pathway in invasion and plaque formation was confirmed by testing the effect of a mutation in the glycolysis gene pfkA. The pfkA mutant was noninvasive and had cell surface alterations as indicated by decreased sensitivity to SDS and an altered lipopolysaccharide profile. The loss of invasion by the csrA and pfkA mutants was due to decreased expression of the S. flexneri virulence factor regulators virF and virB, resulting in decreased production of Shigella invasion plasmid antigens (Ipa). These data indicate that regulation of carbon metabolism and expression of the glycolysis gene pfkA are critical for synthesis of the virulence gene regulators VirF and VirB, and both the glycolytic and gluconeogenic pathways influence steps in S. flexneri invasion and plaque formation.
机译：弗氏志贺氏菌是一种侵袭性细胞内病原体，会侵入并破坏结肠上皮。为了在宿主中蓬勃发展， S。 flexneri 必须适应肠道和真核细胞质内的环境条件，包括可利用的碳源和其他营养素的可变性。我们研究了碳消耗调节剂CsrA和Cra在 S细胞培养模型中的作用。 flexneri 毒力。 CsrA是糖酵解的激活剂，是糖异生的抑制因子， csrA 突变体减少了培养细胞的附着和侵袭。相反，Cra抑制糖酵解并激活糖异生，与野生型菌株相比， cra 突变体的附着力和侵袭力均增加。两种突变体在噬菌斑形成方面均存在缺陷。通过检测糖酵解基因 pfkA 突变的影响，证实了糖酵解途径在侵袭和噬菌斑形成中的重要性。 pfkA 突变体是非侵入性的，并且具有细胞表面改变，如对SDS的敏感性降低和脂多糖谱改变所表明。 csrA 和 pfkA 突变体造成的侵袭损失是由于 S表达降低所致。 flexneri 毒力因子调节剂 virF 和 virB ，导致志贺氏菌入侵质粒抗原（Ipa）的产量降低。这些数据表明碳代谢的调控和糖酵解基因 pfkA 的表达对于合成毒力基因调节因子VirF和VirB至关重要，并且糖酵解途径和糖异生途径均会影响 S的步骤。弗氏菌入侵和斑块形成。

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