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Autophagy and Ubiquitination in Salmonella Infection and the Related Inflammatory Responses

机译:沙门氏菌感染中的自噬和泛素化以及相关的炎症反应

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摘要

Salmonellae are facultative intracellular pathogens that cause globally distributed diseases with massive morbidity and mortality in humans and animals. In the past decades, numerous studies were focused on host defenses against Salmonella infection. Autophagy has been demonstrated to be an important defense mechanism to clear intracellular pathogenic organisms, as well as a regulator of immune responses. Ubiquitin modification also has multiple effects on the host immune system against bacterial infection. It has been indicated that ubiquitination plays critical roles in recognition and clearance of some invading bacteria by autophagy. Additionally, the ubiquitination of autophagy proteins in autophagy flux and inflammation-related substance determines the outcomes of infection. However, many intracellular pathogens manipulate the ubiquitination system to counteract the host immunity. Salmonellae interfere with host responses via the delivery of ~30 effector proteins into cytosol to promote their survival and proliferation. Among them, some could link the ubiquitin-proteasome system with autophagy during infection and affect the host inflammatory responses. In this review, novel findings on the issue of ubiquitination and autophagy connection as the mechanisms of host defenses against Salmonella infection and the subverted processes are introduced.
机译:沙门氏菌是兼性的细胞内病原体,可导致全球分布的疾病,在人类和动物中具有高发病率和死亡率。在过去的几十年中,许多研究集中在针对沙门氏菌感染的宿主防御上。自噬已被证明是清除细胞内致病生物的重要防御机制,也是免疫反应的调节剂。泛素修饰还对宿主抵抗细菌感染的免疫系统具有多种作用。已经表明,泛素化在通过自噬识别和清除某些入侵细菌中起关键作用。另外,自噬通量和炎症相关物质中自噬蛋白的泛素化决定了感染的结果。但是,许多细胞内病原体会操纵泛素化系统来抵消宿主的免疫力。沙门氏菌通过将约30种效应蛋白传递到细胞质中来干扰宿主反应,从而促进它们的存活和增殖。其中,一些可能在感染过程中将泛素-蛋白酶体系统与自噬联系起来,并影响宿主的炎症反应。在这篇综述中,介绍了关于泛素化和自噬连接作为宿主防御沙门氏菌感染和颠覆过程的机制的新发现。

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