School of Public Health, Physiotherapy and Population Science, UCD Centre for Food Safety, UCD Centre for Molecular Innovation and Drug Discovery, University College Dublin , Dublin , Ireland.
Front Immunol. 2014 Oct 7;5:481. doi: 10.3389/fimmu.2014.00481. eCollection 2014.
Salmonella enterica (S. enterica) are Gram-negative bacteria that can invade a broad range of hosts causing both acute and chronic infections. This phenotype is related to its ability to replicate and persist within non-phagocytic host epithelial cells as well as phagocytic dendritic cells and macrophages of the innate immune system. Infection with S. enterica manifests itself through a broad range of clinical symptoms and can result in asymptomatic carriage, gastroenteritis, systemic disease such as typhoid fever and in severe cases, death (1). Exposure to S. enterica serovars Typhi and Paratyphi exhibits clinical symptoms including diarrhea, fatigue, fever, and temperature fluctuations. Other serovars such as the non-typhoidal Salmonella (NTS), of which there are over 2,500, are commonly contracted as, but not limited to, food-borne sources causing gastrointestinal symptoms, which include diarrhea and vomiting. The availability of complete genome sequences for many S. enterica serovars has facilitated research into the genetic determinants of virulence for this pathogen. This work has led to the identification of important bacterial components, including flagella, type III secretion systems, lipopolysaccharides, and Salmonella pathogenicity islands, all of which support the intracellular life cycle of S. enterica. Studies focusing on the host-pathogen interaction have provided insights into receptor activation of the innate immune system. Therefore, characterizing the host-S. enterica interaction is critical to understand the pathogenicity of the bacteria in a clinically relevant context. This review outlines salmonellosis and the clinical manifestations between typhoidal and NTS infections as well as discussing the host immune response to infection and the models that are being used to elucidate the mechanisms involved in Salmonella pathogenicity.
肠沙门氏菌（Salmonella enterica）是一种革兰氏阴性细菌，能够感染广泛宿主，引起急性和慢性感染。这种表型与它在非吞噬宿主上皮细胞以及固有免疫系统中的吞噬树突状细胞和巨噬细胞内复制和持续存在的能力有关。肠沙门氏菌感染表现为广泛的临床症状，可导致无症状携带、胃肠炎、伤寒等全身疾病，在严重情况下可导致死亡（1）。感染肠沙门氏菌血清型 Typhi 和 Paratyphi 表现出腹泻、疲劳、发热和体温波动等临床症状。其他血清型如非伤寒沙门氏菌（NTS），有超过 2500 种，通常通过食物来源等途径感染，引起胃肠道症状，包括腹泻和呕吐。许多肠沙门氏菌血清型的全基因组序列的可用性促进了对该病原体毒力的遗传决定因素的研究。这项工作导致了重要细菌成分的鉴定，包括鞭毛、III 型分泌系统、脂多糖和沙门氏菌致病性岛，所有这些都支持肠沙门氏菌的细胞内生命周期。关注宿主-病原体相互作用的研究提供了对固有免疫系统受体激活的深入了解。因此，描述宿主-肠沙门氏菌的相互作用对于在临床相关背景下理解细菌的致病性至关重要。这篇综述概述了沙门氏菌病和伤寒型与非伤寒型感染之间的临床表现，讨论了宿主对感染的免疫反应以及用于阐明沙门氏菌致病性相关机制的模型。
