肉毒杆菌神经毒素复合物的肠道吸收机制。

T. Matsumura
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引用次数: 0

摘要

肉毒杆菌神经毒素(BoNTs)由厌氧细菌肉毒梭菌及其相关物种产生,引起肉毒中毒,这是一种与高死亡率相关的神经麻痹性疾病。bont通常是通过与包括血凝素(HA)和无毒非血凝素(NTNHA)在内的无毒成分(nap)结合而产生的大蛋白复合物(祖毒素复合物,ptc)。食源性肉毒杆菌中毒是由摄入ptc引起的。胃肠道中的ptc穿过肠上皮屏障,进入血流,到达神经末梢,在那里BoNTs切割囊泡融合所需的SNAREs。因此,bont抑制神经递质释放并导致瘫痪。为了引起食源性肉毒杆菌中毒,bont必须穿过肠上皮屏障。然而,穿越这一屏障的机制尚不清楚。利用体外上皮屏障系统,我们先前发现HA与e -钙粘蛋白的相互作用会导致紧密连接的破坏。此外,我们之前报道了小鼠Peyer's patches (PPs)的滤泡相关上皮(FAE)中的微折叠(M)细胞是A1型BoNT破坏肠上皮屏障的主要部位。在这里,我想展示BoNT复合体的一种巧妙的入侵机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Mechanism of intestinal absorption of botulinum neurotoxin complex].
Botulinum neurotoxins (BoNTs) produced by the anaerobic bacterium Clostridium botulinum and related species cause botulism, a neuroparalytic disease associated with a high mortality. BoNTs are always produced as large protein complexes (progenitor toxin complexes, PTCs) through association with non-toxic components (NAPs) including hemagglutinin (HA) and non-toxic non-hemagglutinin (NTNHA). Food-borne botulism is caused by the ingestion of PTCs. PTCs in the gastrointestinal tract cross the intestinal epithelial barrier, enter the blood stream, and reach the nerve endings, where BoNTs cleave the SNAREs required for vesicle fusion. Consequently, BoNTs inhibit neurotransmitter release and cause paralysis. To cause food-borne botulism, BoNTs must traverse the intestinal epithelial barrier. However, the mechanism used to cross this barrier remains unclear. Using an in vitro epithelial barrier system, we previously showed that the interaction of HA with E-cadherin results in disruption of tight junctions. Furthermore, we previously reported that microfold (M) cells in the follicle-associated epithelium (FAE) of mouse Peyer's patches (PPs) are major sites where type A1 BoNT breaches the intestinal epithelial barrier. Here, I would like to demonstrate an ingenious invasion mechanism of the BoNT complex.
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