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炭疽杆菌的 S 层黏附素 BslA 是炭疽病发病机制的毒力因子。

BslA, the S-layer adhesin of B. anthracis, is a virulence factor for anthrax pathogenesis.

机构信息

Department of Microbiology, University of Chicago, Chicago, IL 60637, USA.

出版信息

Mol Microbiol. 2010 Jan;75(2):324-32. doi: 10.1111/j.1365-2958.2009.06958.x. Epub 2009 Nov 10.

DOI:10.1111/j.1365-2958.2009.06958.x
PMID:19906175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2828814/
Abstract

Microbial pathogens use adhesive surface proteins to bind to and interact with host tissues, events that are universal for the pathogenesis of infectious diseases. A surface adhesin of Bacillus anthracis, the causative agent of anthrax, required to mediate these steps has not been discovered. Previous work identified BslA, an S-layer protein, to be necessary and sufficient for adhesion of the anthrax vaccine strain, Bacillus anthracis Sterne, to host cells. Here we asked whether encapsulated bacilli require BslA for anthrax pathogenesis in guinea pigs. Compared with the highly virulent parent strain B. anthracis Ames, bslA mutants displayed a dramatic increase in the lethal dose and in mean time-to-death. Whereas all tissues of animals infected with B. anthracis Ames contained high numbers of bacilli, only few vegetative forms could be recovered from internal organs of animals infected with the bslA mutant. Surface display of BslA occurred at the poles of encapsulated bacilli and enabled the binding of vegetative forms to host cells. Together these results suggest that BslA functions as the surface adhesin of the anthrax pathogen B. anthracis strain Ames.

摘要

微生物病原体利用粘附表面蛋白与宿主组织结合并相互作用,这些事件是传染病发病机制的普遍现象。炭疽杆菌(炭疽的病原体)的一种表面粘附素,对于介导这些步骤是必需的,但尚未被发现。以前的研究表明,BslA 是一种 S 层蛋白,对于炭疽疫苗株炭疽芽孢杆菌 Sterne 与宿主细胞的粘附是必要且充分的。在这里,我们询问了包被的杆菌是否需要 BslA 才能在豚鼠中引发炭疽病。与高毒力的亲本菌株炭疽芽孢杆菌 Ames 相比,bslA 突变体在致死剂量和平均死亡时间上都有显著增加。虽然感染炭疽芽孢杆菌 Ames 的所有动物组织都含有大量的杆菌,但从感染 bslA 突变体的动物的内脏器官中只能回收很少的营养体形式。BslA 在外层菌的极区显示,并使营养体形式与宿主细胞结合。这些结果表明,BslA 是炭疽病原体炭疽芽孢杆菌菌株 Ames 的表面粘附素。

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