Stevens Mark P, Galyov Edouard E
Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire, United Kingdom.
Int J Med Microbiol. 2004 Apr;293(7-8):549-55. doi: 10.1078/1438-4221-00292.
Intracellular bacterial pathogens have evolved mechanisms to enter and exit eukaryotic cells using the power of actin polymerisation and to subvert the activity of cellular enzymes and signal transduction pathways. The proteins deployed by bacteria to subvert cellular processes often mimic eukaryotic proteins in their structure or function. Studies on the exploitation of host cells by the facultative intracellular pathogen Burkholderia pseudomallei are providing novel insights into the pathogenesis of melioidosis, a serious invasive disease of animals and humans that is endemic in tropical and subtropical areas. B. pseudomallei can invade epithelial cells, survive and proliferate inside phagocytes, escape from endocytic vesicles, form actin-based membrane protrusions and induce host cell fusion. Here we review current understanding of the molecular mechanisms underlying these processes.
细胞内细菌病原体已进化出利用肌动蛋白聚合作用进出真核细胞的机制,并颠覆细胞酶和信号转导途径的活性。细菌用于颠覆细胞过程的蛋白质在结构或功能上常常模仿真核蛋白质。对兼性细胞内病原体伯克霍尔德菌(Burkholderia pseudomallei)利用宿主细胞的研究为类鼻疽病的发病机制提供了新的见解,类鼻疽病是一种严重的侵袭性疾病,在热带和亚热带地区流行于动物和人类中。伯克霍尔德菌可侵入上皮细胞,在吞噬细胞内存活和增殖,从内吞小泡中逃逸,形成基于肌动蛋白的膜突起并诱导宿主细胞融合。在此,我们综述了目前对这些过程潜在分子机制的理解。