C型产气荚膜梭菌致病机理研究进展  

Progress on Pathogenesis Mechanism of Clostridium perfringens Type C

作　　者：李凡飞[1] 张云[2] 李强[1] 赵泽慧 何小丽[1] 许立华[1] 

机构地区：[1]宁夏大学农学院,宁夏银川750021 [2]宁夏大学后勤集团医保中心,宁夏银川750001

出　　处：《动物医学进展》2016年第12期82-85,共4页Progress In Veterinary Medicine

基　　金：宁夏"优质高产奶牛遗传改良与选育"专项(2013NYYZ0501)

摘　　要：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。Clostridiurn perfringens type C causes necrotizing enteritis in humans and some animal species. Type C isolates produce beta toxin （CPB） and alpha toxin （CPA） and most strains produce several other toxins including perfringolysin O （PFO） and TpeL. However, current evidence indicates that CPB is the main virulence factor for type C infections. The rabbit intestinal loop and mouse model experiments showed that C. perfringens type C toxin β gene knockout mutant strain caused the loss of virulence, and the virulence was regained when these mutants were complemented with the wild-type cpb gene. Many type C isolates respond to contact with enterocyte-like Caco-2 cells by producing all toxins, except TpeL, VirS/VirR two-component regulation system （TCRS） proved rapid Caco-2 cell-induced upregulation of CPB and PFO production. The upregulated in vivo transcription of the pfoA and cpb genes was blocked by inactivating the VirR gene,and was reversible by restoring VirR expression. The animal mode experimental research of beta toxin may find effective precautionary measures.

关 键 词：C型产气荚膜梭菌 Β毒素 致病机制 坏死性肠炎 

分 类 号：S852.615[农业科学—基础兽医学]