Recent progress in understanding the pathogenesis of Clostridium perfringens type C infections.
Recent progress in understanding the pathogenesis of Clostridium perfringens type C infections.
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DOI：
10.1016/j.vetmic.2011.02.048
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发表时间：
2011-11-21
影响因子：
3.3
通讯作者：
McClane BA
中科院分区：
文献类型：
--
作者：
Uzal FA;McClane BA
C 型产气荚膜梭菌会引起人类和其他几种动物的坏死性肠炎。 C 型分离株必须至少产生 β 毒素 (CPB) 和 α 毒素 (CPA)，大多数菌株产生几种其他毒素，包括产气荚膜溶血素 O (PFO) 和 TpeL。然而，目前的证据表明，CPB 是 C 型感染的主要毒力因子。大多数证据是基于等基因型 C CPB 敲除突变体在细胞上、兔肠袢和小鼠模型中显示的毒力丧失。当这些突变体与野生型 cpb 基因互补时，这种毒力就会恢复。许多 C 型分离株对与肠细胞样 Caco-2 细胞的密切接触做出反应，产生除 TpeL 之外的所有毒素，其速度比体外生长期间快得多。这种体内效应涉及 cpb、cpb2、pfoA 和 plc 毒素基因的快速转录上调。 Caco-2 细胞诱导的 CPB 和 PFO 产生的快速上调涉及 VirS/VirR 双组分系统，因为 pfoA 和 cpb 基因的体内转录上调被 virR 基因失活所阻断，并且通过互补恢复 VirR 表达而可逆。
Clostridium perfringens type C causes necrotizing enteritis in humans and several other animal species. Type C isolates must produce at least 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. Most of this evidence is based upon the loss of virulence shown by isogenic type C CPB knock out mutants on cells, and also in rabbit intestinal loops and in mouse models. This virulence is regained when these mutants are complemented with the wild-type cpb gene. Many type C isolates respond to close contact with enterocyte-like Caco-2 cells by producing all toxins, except TpeL, much more rapidly than occurs during in vitro growth. This in vivo effect involves rapid transcriptional upregulation of the cpb, cpb2, pfoA and plc toxin genes. Rapid Caco-2 cell-induced upregulation of CPB and PFO production involves the VirS/VirR two-component system, since upregulated in vivo transcription of the pfoA and cpb genes was blocked by inactivating the virR gene and was reversible by complementation to restore VirR expression.
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影响因子：
3.1
作者：
Fisher, Derek J.;Fernandez-Miyakawa, Mariano E.;McClane, Bruce A.
通讯作者：
McClane, Bruce A.
影响因子：
11.8
作者：
Bos, J;Smithee, L;Crutcher, JM
通讯作者：
Crutcher, JM
影响因子：
4.8
作者：
Nagahama, M;Hayashi, S;Sakurai, J
通讯作者：
Sakurai, J
影响因子：
6.4
作者：
MCDONEL, JL;DEMERS, GW
通讯作者：
DEMERS, GW
影响因子：
3.1
作者：
Miyakawa, MEF;Creydt, VP;Ibarra, C
通讯作者：
Ibarra, C