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沙门氏菌的病理生物学、肠道微生物群与宿主先天免疫反应

Pathobiology of salmonella, intestinal microbiota, and the host innate immune response.

作者信息

Santos Renato Lima

机构信息

Departamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária, Universidade Federal de Minas Gerais , Belo Horizonte , Brazil.

出版信息

Front Immunol. 2014 May 26;5:252. doi: 10.3389/fimmu.2014.00252. eCollection 2014.

DOI:10.3389/fimmu.2014.00252
PMID:24904595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4033611/
Abstract

Salmonella is a relevant pathogen under a clinical and public health perspective. Therefore, there has been a significant scientific effort to learn about pathogenic determinants of this pathogen. The clinical relevance of the disease, associated with the molecular tools available to study Salmonella as well as suitable animal models for salmonellosis, have provided optimal conditions to drive the scientific community to generate a large expansion of our knowledge about the pathogenesis of Salmonella-induced enterocolitis that took place during the past two decades. This research effort has also generated a wealth of information on the host immune mechanisms that complements gaps in the fundamental research in this area. This review focus on how the interaction between Salmonella, the microbiota and intestinal innate immunity leads to disease manifestation. As a highly successful enteropathogen, Salmonella actively elicits a robust acute intestinal inflammatory response from the host, which could theoretically lead to the pathogen demise. However, Salmonella has evolved redundant molecular machineries that renders this pathogen highly adapted to the inflamed intestinal environment, in which Salmonella is capable of outcompete resident commensal organisms. The adaptation of Salmonella to the inflamed intestinal lumen associated with the massive inflammatory response that leads to diarrhea, generate perfect conditions for transmission of the pathogen. These conditions illustrate the complexity of the co-evolution and ecology of the pathogen, commensals, and the host.

摘要

从临床和公共卫生角度来看,沙门氏菌是一种重要的病原体。因此,为了解该病原体的致病决定因素,人们付出了巨大的科学努力。与研究沙门氏菌可用的分子工具以及沙门氏菌病合适的动物模型相关的该疾病的临床相关性,为推动科学界大幅扩展我们对过去二十年中沙门氏菌诱导的小肠结肠炎发病机制的认识提供了最佳条件。这项研究工作还产生了大量关于宿主免疫机制的信息,填补了该领域基础研究的空白。本综述聚焦于沙门氏菌、微生物群和肠道固有免疫之间的相互作用如何导致疾病表现。作为一种非常成功的肠道病原体,沙门氏菌会积极引发宿主强烈的急性肠道炎症反应,理论上这可能导致病原体死亡。然而,沙门氏菌已经进化出冗余的分子机制,使其高度适应炎症性肠道环境,在这种环境中沙门氏菌能够胜过常驻共生生物。沙门氏菌对与导致腹泻的大规模炎症反应相关的炎症性肠腔的适应,为病原体的传播创造了完美条件。这些情况说明了病原体、共生生物和宿主共同进化与生态的复杂性。

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Mucosal innate immune cells regulate both gut homeostasis and intestinal inflammation.黏膜固有免疫细胞调节肠道稳态和肠道炎症。
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The Protective Effect of on Infection Induced Damage to Intestinal Mucosa.[具体物质]对[具体病原体]感染所致肠黏膜损伤的保护作用
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