论文部分内容阅读
C型产气荚膜梭菌能够引起人类和一些动物的坏死性肠炎。该菌能产生α外毒素和β外毒素,大部分该菌菌株也能分泌出产气梭菌细胞溶素O(PFO)和TpeL。试验证明β外毒素是C型产气荚膜梭菌的主要致病毒素。在兔子肠襻和小鼠模型试验中发现,通过细胞中同源基因C型产气荚膜梭菌β毒素敲除基因突变株而导致该菌株失去毒力。当野生型β毒素基因补充这些突变体时毒素的活力将会复活。大多数C型产气荚膜梭菌产生的所有毒素(除TpeL外)都易与肠癌(Caco-2)细胞紧密结合并发生反应,比它在体外生长更加迅速。VirS/virR双组分调节系统(TCRS)被证明是在Coca-2细胞中导致β毒素和PFO产生快速上调。当virR基因被抑制时,pfoA和β毒素基因的表达也会受阻,这种系统是可逆的,virR表达时会恢复。通过β毒素作用于动物模型的试验研究,来寻找有效的预防措施。
Clostridium perfringens type C is capable of causing necrotic enteritis in humans and some animals. The bacteria produce alpha exotoxin and beta exotoxin, and most of the strains also secrete Clostridium aeruginosa cytolysin (PFO) and TpeL. It has been demonstrated that beta exotoxin is the major causative toxin of Clostridium perfringens type C. In the rabbit gut and mouse model tests, the strain was found to lose virulence by mutating the homologous gene C-type Clostridium perfringens beta-toxin knockout gene in the cell. The viability of toxins will be revived when wild-type beta toxin genes complement these mutants. Most of the toxins produced by most Clostridium perfringens type C (except TpeL) tend to bind and react with Caco-2 cells more rapidly than it does in vitro. The VirS / virR two-part regulatory system (TCRS) proved to result in the rapid up-regulation of beta toxin and PFO production in Coca-2 cells. When the virR gene is repressed, the expression of the pfoA and beta toxin genes is also hindered. This system is reversible and recovers when virR is expressed. By β-toxin in animal models of experimental study to find effective preventive measures.