Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Department of Biochemistry, University of Toronto, Ontario, Canada.
IUBMB Life. 2018 May;70(5):384-392. doi: 10.1002/iub.1737. Epub 2018 Mar 23.
Innate immunity relies on the effective recognition and elimination of pathogenic microorganisms. This entails sequestration of pathogens into phagosomes that promptly acquire microbicidal and degradative properties. This complex series of events, which involve cytoskeletal reorganization, membrane remodeling and the activation of multiple enzymes, is orchestrated by lipid signaling. To overcome this immune response, intracellular pathogens acquired mechanisms to subvert phosphoinositide-mediated signaling and use host lipids, notably cholesterol, as nutrients. We present brief overviews of the role of phosphoinositides in phagosome formation and maturation as well as of cholesterol handling by host cells, and selected Salmonella, Shigella, Chlamydia and Mycobacterium tuberculosis to exemplify the mechanisms whereby intracellular pathogens co-opt lipid metabolism in host cells. © 2018 IUBMB Life, 70(5):384-392, 2018.
先天免疫依赖于对病原微生物的有效识别和清除。这需要将病原体隔离在吞噬体中,吞噬体迅速获得杀菌和降解特性。这一系列复杂的事件,涉及细胞骨架重组、膜重塑和多种酶的激活,由脂质信号协调。为了克服这种免疫反应,细胞内病原体获得了颠覆磷酯酰肌醇介导的信号转导并利用宿主脂质(特别是胆固醇)作为营养物质的机制。我们简要概述了磷酯酰肌醇在吞噬体形成和成熟中的作用以及宿主细胞处理胆固醇的作用,并选择了沙门氏菌、志贺氏菌、衣原体和结核分枝杆菌来说明细胞内病原体如何在宿主细胞中篡夺脂质代谢的机制。 © 2018 IUBMB Life, 70(5):384-392, 2018.