Departamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Trends Microbiol. 2009 Nov;17(11):498-506. doi: 10.1016/j.tim.2009.08.008. Epub 2009 Oct 12.
The lower gastrointestinal tract is densely populated with resident microbial communities (microbiota), which do not elicit overt host responses but rather provide benefit to the host, including niche protection from pathogens. However, introduction of bacteria into the underlying tissue evokes acute inflammation. Non-typhoidal Salmonella serotypes (NTS) elicit this stereotypic host response by actively penetrating the intestinal epithelium and surviving in tissue macrophages. Initial responses generated by bacterial host cell interaction are amplified in tissue through the interleukin (IL)-18/interferon-gamma and IL-23/IL-17 axes, resulting in the activation of mucosal barrier functions against NTS dissemination. However, the pathogen is adapted to survive antimicrobial defenses encountered in the lumen of the inflamed intestine. This strategy enables NTS to exploit inflammation to outcompete the intestinal microbiota, and promotes the Salmonella transmission by the fecal/oral route.
下胃肠道中聚居着大量常驻微生物群落（微生物群），这些微生物群落不会引起宿主明显的反应，而是对宿主有益，包括为宿主提供免受病原体侵害的小生境。然而，将细菌引入到下层组织会引发急性炎症。非伤寒型沙门氏菌血清型（NTS）通过主动穿透肠上皮细胞并在组织巨噬细胞中存活，引发这种典型的宿主反应。细菌与宿主细胞相互作用产生的初始反应通过白细胞介素（IL）-18/干扰素-γ和 IL-23/IL-17 轴在组织中放大，导致黏膜屏障功能被激活以抵抗 NTS 的传播。然而，病原体适应了在发炎肠道的腔中遇到的抗菌防御。这种策略使 NTS 能够利用炎症来与肠道微生物群竞争，并通过粪便/口腔途径促进沙门氏菌的传播。
