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肺炎军团菌感染中的先天感应和细胞自主抵抗途径。

Innate sensing and cell-autonomous resistance pathways in Legionella pneumophila infection.

机构信息

Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Augustenburger Platz 1, 13353 Berlin, Germany.

Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Augustenburger Platz 1, 13353 Berlin, Germany; German Center for Lung Research (DZL), Germany.

出版信息

Int J Med Microbiol. 2018 Jan;308(1):161-167. doi: 10.1016/j.ijmm.2017.10.004. Epub 2017 Oct 27.

DOI:10.1016/j.ijmm.2017.10.004
PMID:29097162
Abstract

Legionella pneumophila is a facultative intracellular bacterium which can cause a severe pneumonia called Legionnaires' disease after inhalation of contaminated water droplets and replication in alveolar macrophages. The innate immune system is generally able to sense and -in most cases- control L. pneumophila infection. Comorbidities and genetic risk factors, however, can compromise the immune system and high infection doses might overwhelm its capacity, thereby enabling L. pneumophila to grow and disseminate inside the lung. The innate immune system mediates sensing of L. pneumophila by employing e.g. NOD-like receptors (NLRs), Toll-like receptors (TLRs), as well as the cGAS/STING pathway to stimulate death of infected macrophages as well as production of proinflammatory cytokines and interferons (IFNs). Control of pulmonary L. pneumophila infection is largely mediated by inflammasome-, TNFα- and IFN-dependent macrophage-intrinsic resistance mechanisms. This article summarizes the current knowledge of innate immune responses to L. pneumophila infection in general, and of macrophage-intrinsic defense mechanisms in particular.

摘要

嗜肺军团菌是一种兼性细胞内细菌,吸入含有污染水滴的飞沫并在肺泡巨噬细胞内复制后,可引起一种称为军团病的严重肺炎。先天免疫系统通常能够感知并在大多数情况下控制嗜肺军团菌感染。然而,合并症和遗传风险因素会损害免疫系统,高感染剂量可能会超过其能力,从而使嗜肺军团菌能够在肺部内生长和传播。先天免疫系统通过例如 NOD 样受体 (NLRs)、Toll 样受体 (TLRs) 以及 cGAS/STING 途径来感知嗜肺军团菌的感染,从而刺激受感染的巨噬细胞死亡以及产生促炎细胞因子和干扰素 (IFNs)。肺部嗜肺军团菌感染的控制主要通过炎性小体、TNFα 和 IFN 依赖的巨噬细胞内在抵抗机制来介导。本文总结了先天免疫系统对嗜肺军团菌感染的一般反应以及巨噬细胞内在防御机制的最新知识。

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