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首页> 外文期刊>Infection and immunity >The Clostridium difficile Dlt Pathway Is Controlled by the Extracytoplasmic Function Sigma Factor σV in Response to Lysozyme
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The Clostridium difficile Dlt Pathway Is Controlled by the Extracytoplasmic Function Sigma Factor σV in Response to Lysozyme

机译：难溶梭状芽胞杆菌Dlt通路受胞外功能西格玛因子σV响应溶菌酶的控制。

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Clostridium difficile (also known as Peptoclostridium difficile) is a major nosocomial pathogen and a leading cause of antibiotic-associated diarrhea throughout the world. Colonization of the intestinal tract is necessary for C. difficile to cause disease. Host-produced antimicrobial proteins (AMPs), such as lysozyme, are present in the intestinal tract and can deter colonization by many bacterial pathogens, and yet C. difficile is able to survive in the colon in the presence of these AMPs. Our prior studies established that the Dlt pathway, which increases the surface charge of the bacterium by addition of d-alanine to teichoic acids, is important for C. difficile resistance to a variety of AMPs. We sought to determine what genetic mechanisms regulate expression of the Dlt pathway. In this study, we show that a dlt null mutant is severely attenuated for growth in lysozyme and that expression of the dltDABC operon is induced in response to lysozyme. Moreover, we found that a mutant lacking the extracytoplasmic function (ECF) sigma factor σV does not induce dlt expression in response to lysozyme, indicating that σV is required for regulation of lysozyme-dependent d-alanylation of the cell wall. Using reporter gene fusions and 5′ RACE (rapid amplification of cDNA ends) analysis, we identified promoter elements necessary for lysozyme-dependent and lysozyme-independent dlt expression. In addition, we observed that both a sigV mutant and a dlt mutant are more virulent in a hamster model of infection. These findings demonstrate that cell wall d-alanylation in C. difficile is induced by lysozyme in a σV-dependent manner and that this pathway impacts virulence in vivo.
机译：艰难梭菌（又称艰难梭菌）是世界上主要的医院病原体和抗生素相关性腹泻的主要原因。肠道菌落对于艰难梭菌引起疾病是必需的。宿主产生的抗微生物蛋白（AMP）（例如溶菌酶）存在于肠道中，可以阻止许多细菌性病原体的定殖，而艰难梭菌仍能够在这些AMP存在的情况下在结肠中存活。我们先前的研究表明，Dlt途径通过向D-choicic酸中添加d-丙氨酸来增加细菌的表面电荷，对艰难梭菌对多种AMP的抗性很重要。我们试图确定哪些遗传机制调节Dlt途径的表达。在这项研究中，我们显示了 dlt 无效突变体在溶菌酶中的生长受到严重减毒，并且 dltDABC 操纵子的表达被诱导以响应溶菌酶。此外，我们发现缺少胞浆外功能（ECF）σ因子 V 的突变体不会诱导溶菌酶引起 dlt 表达，表明σ V < / sup>是调节细胞壁溶菌酶依赖性d-丙氨酸化所必需的。使用报告基因基因融合和5'RACE（cDNA末端的快速扩增）分析，我们鉴定了依赖溶菌酶和不依赖溶菌酶的 dlt 表达所必需的启动子元件。此外，我们观察到 sigV 突变体和 dlt 突变体在仓鼠感染模型中都更具毒性。这些发现表明，溶菌酶以σ V 依赖性方式诱导了艰难梭菌细胞壁的d-丙氨酸化，并且该途径影响了体内的毒力。

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