Clostridium perfringens enterotoxin and intestinal tight junctions.
Clostridium perfringens enterotoxin and intestinal tight junctions.
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产气荚膜梭菌肠毒素和肠道紧密连接。
DOI：
10.1016/s0966-842x(00)01724-8
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发表时间：
2000
影响因子：
15.9
通讯作者：
McClane,BA
中科院分区：
文献类型：
--
作者：
McClane,BA
TJ上的CPE片段(或CPE)代表了天然CPE的主要启动GI作用。他们观察到，只有当C-CPE添加到MDCK细胞的基侧时，C-CPE才会对MDCK细胞的TJ链和细胞旁通透性产生影响。正如他们指出的那样，这引起了人们的重大怀疑，即非细胞毒性CPE片段引起的TJ变化和通透性变化能否解释天然CPE的主要GI作用，因为CPE最初存在于胃肠道疾病期间的肠腔中，因此首先与肠上皮的顶面相互作用。相反，当加入到肠上皮顶端2-4，7时，天然CPE迅速诱导细胞毒性反应和组织病理学损伤。有趣的是，已经独立观察到(C.Rahner等人，未发表)，必须将天然CPE加入到大鼠肝细胞的基底外侧才能对TJs产生作用。这一观察结果，再加上CPE最初与根尖膜相互作用的事实，强烈表明即使是完全细胞毒性的天然CPE诱导的TJ效应也不太可能代表这种肠毒素在胃肠道疾病中的启动作用。然而，CPE(或C-CPE)从基底侧诱导TJ效应的能力可能会导致CPE诱导的液体和电解质损失，一旦细胞毒性导致的组织病理损伤为肠毒素提供了进入某些肠道细胞基外侧表面的途径。13和Rahner等人。不可否认，由于使用了略有不同的非细胞毒性羧基末端CPE片段和相当不同的模型系统(这可能反映也可能不反映肠道中发生的情况)，14的情况很复杂。尽管如此，这些研究还是提出了一些关于CPE-TJ蛋白相互作用的问题。例如，为什么天然CPE(或CPE片段)只在
CPE fragments (or CPE) on TJs represent the major initiating GI action of native CPE. They observed that C-CPE effects on TJ strands and paracellular permeability of MDCK cells occurred only when C-CPE was added to the basolateral side of those cells. As they noted13, this raises significant doubts that the TJ changes and permeability alterations induced by non-cytotoxic CPE fragments could explain the primary GI action of native CPE, as CPE is initially present in the intestinal lumen during GI disease and thus interacts first with the apical surface of the intestinal epithelium. By contrast, native CPE quickly induces a cytotoxic response and histopathological damage when added to the apical side of the intestinal epithelium2–4, 7. Interestingly, it has been independently observed (C. Rahner et al., unpublished) that native CPE must be added to the basolateral side of rat liver cells to obtain effects on TJs. This observation, coupled with the fact that CPE initially interacts with apical membranes, strongly suggests that even the TJ effects induced by fully cytotoxic, native CPE are unlikely to represent the initiating effect of this enterotoxin in GI disease. However, the ability of CPE (or C-CPE) to induce TJ effects from the basolateral side could conceivably contribute to CPE-induced fluid and electrolyte losses later in disease, once cytotoxicity-induced histopathological damage provides the enterotoxin with access to the basolateral surface of some intestinal cells.Future directions Comparison of data from the studies of Sonoda et al. 13 and Rahner et al. 14 is admittedly complicated by their use of slightly different noncytotoxic carboxy-terminal CPE fragments and considerably different model systems (which may or may not reflect what is happening in the intestines). Nonetheless, these studies have raised several questions regarding CPE–TJ protein interactions. For example, why does native CPE (or CPE fragments) only induce TJ rearrangements in
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有证据表明，具有受体样特性的约 50 kDa 哺乳动物质膜蛋白介导特异性结合产气荚膜梭菌肠毒素的两亲性。
DOI：
--
发表时间：
1994
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Wieckowski,EU;Wnek,AP;McClane,BA
通讯作者：
McClane,BA
A 型产气荚膜梭菌肠毒素会引起兔回肠组织损伤和积液。
DOI：
--
发表时间：
1994
期刊：
Journal of diarrhoeal diseases research
影响因子：
--
作者：
Sherman,S;Klein,E;McClane,BA
通讯作者：
McClane,BA
DOI：
10.1083/jcb.136.6.1239
发表时间：
1997-03-24
期刊：
The Journal of cell biology
影响因子：
--
作者：
Katahira J;Inoue N;Horiguchi Y;Matsuda M;Sugimoto N
通讯作者：
Sugimoto N
产气荚膜梭菌肠毒素的最新进展。
DOI：
--
发表时间：
2000
期刊：
Journal of natural toxins.
影响因子：
--
作者：
Sarker,MR;Singh,U;McClane,BA
通讯作者：
McClane,BA