Department of Molecular Genetics & Microbiology & Center for Microbial Pathogenesis Duke University Medical Center, 272 Jones Building, Box 3580, Durham, NC 27710, USA.
Future Microbiol. 2010 Aug;5(8):1219-32. doi: 10.2217/fmb.10.77.
The obligate intracellular bacterial pathogen Chlamydia trachomatis is a major cause of blindness and sexually transmitted diseases. Like the enteric pathogens Salmonella and Shigella, Chlamydia injects effector proteins into epithelial cells to initiate extensive remodeling of the actin cytoskeleton at the bacterial attachment site, which culminates in the engulfment of the bacterium by plasma membrane extensions. Numerous Salmonella and Shigella effectors promote this remodeling by activating Rho GTPases and tyrosine kinase signaling cascades and by directly manipulating actin dynamics. Recent studies indicate that similar host-cell alterations occur during Chlamydia invasion, but few effectors are known. The identification of additional Chlamydia effectors and the elucidation of their modes of function are critical steps towards an understanding of how this clinically important pathogen breaches epithelial surfaces and causes infection.
专性细胞内细菌病原体沙眼衣原体是导致失明和性传播疾病的主要原因。与肠道病原体沙门氏菌和志贺氏菌一样，沙眼衣原体将效应蛋白注入上皮细胞，在细菌附着部位引发广泛的肌动蛋白细胞骨架重排，最终导致细菌被质膜延伸包裹。许多沙门氏菌和志贺氏菌效应蛋白通过激活 Rho GTPases 和酪氨酸激酶信号级联以及直接操纵肌动蛋白动力学来促进这种重排。最近的研究表明，在沙眼衣原体入侵过程中也会发生类似的宿主细胞改变，但已知的效应蛋白很少。鉴定更多的沙眼衣原体效应蛋白及其功能模式是理解这种临床上重要的病原体如何突破上皮表面并引起感染的关键步骤。
