The complex interactions between Clostridium perfringens enterotoxin and epithelial tight junctions
The complex interactions between Clostridium perfringens enterotoxin and epithelial tight junctions
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DOI：
10.1016/s0041-0101(01)00164-7
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发表时间：
2001-11-01
期刊：
影响因子：
2.8
通讯作者：
McClane, BA
中科院分区：
文献类型：
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作者：
McClane, BA
产气荚膜梭菌肠毒素（CPE）是产气荚膜梭菌A型食物中毒和抗生素相关性腹泻的腹泻症状的原因。CPE蛋白由单个35 kDa多肽组成，具有c端受体结合区和n端毒性结构域。在适当的条件下，CPE可以与上皮紧密连接的结构成分相互作用，包括某些claudin和occludin。这些相互作用可以影响紧密连接的结构和功能，从而改变细胞旁通透性，并（可能）导致cpe诱导的腹泻。然而，CPE的紧密连接效应需要细胞损伤作为先决条件。CPE通过其细胞毒性活性诱导细胞损伤，这是由于形成类似于155 kDa的CPE复合物（可能对应于一个孔）引起的质膜通透性改变。因此，CPE似乎是一种双功能毒素，首先诱导质膜通透性改变；利用由此产生的细胞损伤，CPE随后获得紧密连接蛋白并影响紧密连接的结构和功能。(C) 2001年Elsevier Science Ltd.出版
Clostridium perfringens enterotoxin (CPE) is responsible for the diarrheal symptoms of C. perfringens type A food poisoning and anti biotic-associated diarrhea. The CPE protein consists of a single 35 kDa polypeptide with a C-terminal receptor-binding region and an N-terminal toxicity domain. Under appropriate conditions, CPE can interact with structural components of the epithelial tight junctions, including certain claudins and occludin. Those interactions can affect tight junction structure and function, thereby altering paracellular permeability and (possibly) contributing to CPE-induced diarrhea. However, the tight junction effects of CPE require cellular damage as a prerequisite. CPE induces cellular damage via its cytotoxic activity, which results from plasma membrane permeability alterations caused by formation of a similar to 155 kDa CPE-containing complex that may correspond to a pore. Thus, CPE appears to be a bifunctional toxin that first induces plasma membrane permeability alterations; using the resultant cell damage, CPE then gains access to tight junction proteins and affects tight junction structure and function. (C) 2001 Published by Elsevier Science Ltd.