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艰难梭菌感染的发病机制。

Pathogenesis of Clostridium difficile infection.

作者信息

Borriello S P

机构信息

Central Public Health Laboratory, London, UK.

出版信息

J Antimicrob Chemother. 1998 May;41 Suppl C:13-9. doi: 10.1093/jac/41.suppl_3.13.

Abstract

Clostridium difficile produces two major toxins referred to as toxins A and B. These are thought to be primarily responsible for the virulence of the bacterium and the major contributors to the pathogenesis of antibiotic-associated gastrointestinal disease. The molecular organization and control of expression of toxins A and B is now starting to be understood, and the cellular mechanism of action of both toxins, glucosylation of Rho family proteins, has been discovered. Other factors, such as production of proteolytic and hydrolytic enzymes, expression of fimbriae and flagella, chemotaxis and adhesion to gut receptors, and production of capsule, may all play a part in pathogenesis by facilitating colonization or by directly contributing to tissue damage, or both. Differential expression between strains of various combinations of these colonization and virulence factors may explain the apparent variability in virulence of C. difficile strains.

摘要

艰难梭菌产生两种主要毒素,称为毒素A和毒素B。这些毒素被认为是该细菌毒力的主要原因,也是抗生素相关性胃肠道疾病发病机制的主要促成因素。毒素A和B的分子结构和表达调控目前已开始被了解,并且已经发现了这两种毒素的细胞作用机制,即Rho家族蛋白的糖基化。其他因素,如蛋白水解酶和水解酶的产生、菌毛和鞭毛的表达、趋化作用以及与肠道受体的黏附,还有荚膜的产生,都可能通过促进定植或直接导致组织损伤,或两者兼而有之,在发病机制中发挥作用。这些定植和毒力因子的各种组合在不同菌株间的差异表达,可能解释了艰难梭菌菌株毒力明显不同的原因。

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