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首页> 外文期刊>Infection and immunity >Role of the Agr-Like Quorum-Sensing System in Regulating Toxin Production by Clostridium perfringens Type B Strains CN1793 and CN1795
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Role of the Agr-Like Quorum-Sensing System in Regulating Toxin Production by Clostridium perfringens Type B Strains CN1793 and CN1795

机译：类似于Agr的群体感应系统在产气荚膜梭菌B型菌株CN1793和CN1795调节毒素产生中的作用

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Clostridium perfringens type B causes enteritis and enterotoxemia in domestic animals. By definition, these bacteria must produce alpha toxin (CPA), beta toxin (CPB) and epsilon toxin (ETX) although most type B strains also produce perfringolysin O (PFO) and beta2 toxin (CPB2). A recently identified Agr-like quorum-sensing (QS) system in C. perfringens controls all toxin production by surveyed type A, C, and D strains, but whether this QS is involved in regulating toxin production by type B strains has not been explored. Therefore, the current study introduced agrB null mutations into type B strains CN1795 and CN1793. Both type B agrB null mutants exhibited reduced levels of CPB, PFO, and CPA in their culture supernatants, and this effect was reversible by complementation. The reduced presence of CPB in culture supernatant involved decreased cpb transcription. In contrast, the agrB null mutants of both type B strains retained wild-type production levels of ETX and CPB2. In a Caco-2 cell model of enteritis, culture supernatants of the type B agrB null mutants were less cytotoxic than supernatants of their wild-type parents. However, in an MDCK cell in vitro model for enterotoxemic effects, supernatants from the agrB null mutants or wild-type parents were equally cytotoxic after trypsin activation. Coupling these and previous results, it is now evident that strain-dependent variations exist in Agr-like QS system regulation of C. perfringens toxin production. The cell culture results further support a role for trypsin in determining which toxins contribute to disease involving type B strains.
机译：B型产气荚膜梭菌会引起家畜肠炎和肠毒素血症。根据定义，这些细菌必须产生α毒素（CPA），β毒素（CPB）和epsilon毒素（ETX），尽管大多数B型菌株也产生全氟丁酸溶血素O（PFO）和β2毒素（CPB2）。最近确定的产气荚膜梭菌中的类似Agr的群体感应（QS）系统可控制所调查的A，C和D型菌株的所有毒素产生，但是尚未探究该QS是否参与调节B型菌株的毒素产生。 。因此，当前的研究将 agrB 无效突变引入B型菌株CN1795和CN1793。这两个B型 agrB 无效突变体在其培养上清液中均显示出降低的CPB，PFO和CPA水平，并且这种作用可以通过互补来逆转。 CPB在培养上清液中的存在减少涉及 cpb 转录的降低。相反，两种B型菌株的 agrB 空突变体均保留了ETX和CPB2的野生型生产水平。在肠炎的Caco-2细胞模型中，B型 agrB 空突变体的培养上清液比其野生型亲本的上清液具有较低的细胞毒性。但是，在具有肠毒素作用的MDCK细胞“体外”模型中，胰蛋白酶激活后，来自 agrB 无效突变体或野生型亲本的上清液具有相同的细胞毒性。结合这些结果和以前的结果，现在很明显，菌株依赖性变异存在于产气荚膜梭菌毒素生产的类似Agr的QS系统调节中。细胞培养结果进一步支持胰蛋白酶在确定哪些毒素促成涉及B型菌株的疾病中的作用。

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