Gastrointestinal phase of Listeria monocytogenes infection
Gastrointestinal phase of Listeria monocytogenes infection
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DOI：
10.1111/j.1365-2672.2005.02559.x
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发表时间：
2005-01-01
影响因子：
4
通讯作者：
Hill, C
中科院分区：
文献类型：
--
作者：
Gahan, CGM;Hill, C
多年来，革兰氏阳性菌胞内食源性致病菌单核细胞增生李斯特菌一直被用作研究胞内寄生的模式生物。虽然细胞致病的基本机制已阐明了一系列优雅的研究，最近的研究已经开始集中在胃肠道（GI）阶段的L。单核细胞增生感染。对人类疾病暴发的流行病学研究现在表明，该病原体可在没有侵入性疾病和相关死亡的情况下引起胃肠炎。此外，病原体具有在感染小鼠的胆囊中定殖的能力，这可能在发病过程中作为重要的感染焦点。病原体在胃肠道的各种微环境中存活的能力对于引起食源性感染是必不可少的。病原体在胃酸中的存活需要谷氨酸脱羧酶（GAD）系统。此外，肉毒碱摄取系统OpuC对于鼠胃肠道内的适应和随后的侵袭性疾病是必不可少的。胆盐在体外和体内的存活需要许多机制，包括胆盐水解酶（Bsh）和最近描述的胆汁排阻系统，BilE（以前的OpuB）。最后，许多这些系统（包括Bsh、OpuC和BilE）受交替应力σ因子Sigma B和毒力基因表达调节因子PrfA的调节。
For many years the Gram-positive facultatively intracellular food- borne pathogen Listeria monocytogenes has been used as a model organism for the study of intracellular parasitism. Whilst the basic mechanisms of cellular pathogenesis have been elucidated by a series of elegant studies, recent research has begun to focus upon the gastrointestinal (GI) phase of L. monocytogenes infection. Epidemiological studies of outbreaks of human disease now demonstrate that the pathogen can cause gastroenteritis in the absence of invasive disease and associated mortality. Furthermore, the pathogen has the ability to colonize the gallbladder in infected mice and this may function as a significant focus of infection during pathogenesis. The ability of the pathogen to survive within the various microenvironments of the GI tract is essential for the causation of food- borne infection. Survival of the pathogen within gastric acid requires the glutamate decarboxylase ( GAD) system. In addition, the carnitine uptake system, OpuC is essential for adaptation within the murine GI tract and subsequent invasive disease. Survival of bile salts both in vitro and in vivo requires a number of mechanisms including bile salt hydrolase (Bsh) and the recently described bile exclusion system, BilE ( previously OpuB). Finally a number of these systems (including Bsh, OpuC and BilE) are regulated by both the alternative stress sigma factor, Sigma B and by the regulator of virulence gene expression, PrfA.