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食源性病原体的空泡逃逸。

Vacuolar escape of foodborne bacterial pathogens.

机构信息

Department of Molecular Immunology and Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, 9722GR Groningen, The Netherlands

Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, 9625GA Nijmegen, The Netherlands.

出版信息

J Cell Sci. 2020 Sep 1;134(5):jcs247221. doi: 10.1242/jcs.247221.

Abstract

The intracellular pathogens , , spp. and are major causes of foodborne illnesses. Following the ingestion of contaminated food or beverages, pathogens can invade epithelial cells, immune cells and other cell types. Pathogens survive and proliferate intracellularly via two main strategies. First, the pathogens can remain in membrane-bound vacuoles and tailor organellar trafficking to evade host-cell defenses and gain access to nutrients. Second, pathogens can rupture the vacuolar membrane and proliferate within the nutrient-rich cytosol of the host cell. Although this virulence strategy of vacuolar escape is well known for and spp., it has recently become clear that and spp. also gain access to the cytosol, and that this is important for their survival and growth. In this Review, we discuss the molecular mechanisms of how these intracellular pathogens rupture the vacuolar membrane by secreting a combination of proteins that lyse the membranes or that remodel the lipids of the vacuolar membrane, such as phospholipases. In addition, we also propose that oxidation of the vacuolar membrane also contributes to cytosolic pathogen escape. Understanding these escape mechanisms could aid in the identification of new therapeutic approaches to combat foodborne pathogens.

摘要

胞内病原体、、 属和 属是食源性疾病的主要原因。食入被污染的食物或饮料后,病原体可以侵入上皮细胞、免疫细胞和其他细胞类型。病原体通过两种主要策略在细胞内存活和增殖。首先,病原体可以留在膜结合的小泡中,并调整细胞器运输以逃避宿主细胞防御并获得营养。其次,病原体可以破坏液泡膜并在宿主细胞富含营养的细胞质中增殖。尽管这种液泡逃逸的毒力策略对于 和 属是众所周知的,但最近已经清楚, 和 属也可以进入细胞质,这对于它们的存活和生长很重要。在这篇综述中,我们讨论了这些胞内病原体通过分泌一组裂解膜或重塑液泡膜脂质的蛋白质来破坏液泡膜的分子机制,例如磷脂酶。此外,我们还提出液泡膜的氧化也有助于胞质病原体的逃逸。了解这些逃逸机制有助于确定新的治疗方法来对抗食源性病原体。

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