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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mucosal penetration primes Vibrio cholerae for host colonization by repressing quorum sensing
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Mucosal penetration primes Vibrio cholerae for host colonization by repressing quorum sensing

机译：粘膜渗透通过抑制群体感应而引发霍乱弧菌，使其寄居于宿主

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摘要

To successfully infect a host and cause the diarrheal disease cholera. Vibrio cholerae must penetrate the intestinal mucosal layer and express virulence genes. Previous studies have demonstrated that the transcriptional regulator HapR, which is part of the quorum sensing network in V. cholerae, represses the expression of virulence genes. Here, we show that hapR expression is also modulated by the regulatory network that governs flagellar assembly. Specifically, FliA, which is the alternative σ-factor (σ~(28)) that activates late-class flagellin genes in V. cholerae, represses hapR expression. In addition, we show that mucin penetration by V. cholerae is sufficient to break flagella and so cause the secretion of FlgM, the anti-σ factor that inhibits FliA activity. During initial colonization of host intestinal tissue, hapR expression is repressed because of low cell density. However, full repression of hapR expression does not occur in fliA mutants, which results in attenuated colonization. Our results suggest that V. cholerae uses flagellar machinery to sense particular intestinal signals before colonization and enhance the expression of virulence genes by modulating the output of quorum sensing signaling.
机译：要成功感染宿主并引起霍乱腹泻病。霍乱弧菌必须穿透肠道粘膜层并表达毒力基因。先前的研究表明，霍乱弧菌群体感应网络中的转录调节子HapR抑制了毒力基因的表达。在这里，我们显示hapR表达也受到控制鞭毛装配的调节网络的调节。具体地说，FliA是激活霍乱弧菌中晚期鞭毛蛋白基因的另一种σ因子（σ〜（28）），可抑制hapR表达。此外，我们显示霍乱弧菌的粘蛋白渗透足以破坏鞭毛，从而引起FlgM的分泌，FlgM是抑制FliA活性的抗σ因子。在宿主肠组织的最初定殖期间，由于细胞密度低，hapR表达受到抑制。但是，在fliA突变体中不会完全抑制hapR表达，这会导致定植减弱。我们的结果表明，霍乱弧菌利用鞭毛机制在定植前感测特定的肠道信号，并通过调节群体感应信号的输出来增强毒力基因的表达。

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