Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.
Cell Microbiol. 2018 Aug;20(8):e12861. doi: 10.1111/cmi.12861. Epub 2018 Jun 20.
Many microbial pathogens co-opt or perturb host membrane trafficking pathways. This review covers recent examples in which microbes interact with host exocytosis, the fusion of intracellular vesicles with the plasma membrane. The bacterial pathogens Listeria monocytogenes and Staphylococcus aureus subvert recycling endosomal pathways of exocytosis in order to induce their entry into human cells. By contrast, entry of the protozoan pathogen Trypanosoma cruzi or the virus adenovirus into host cells involves exploitation of lysosomal exocytosis. Toxins produced by Bacillus anthracis or Vibrio cholerae interfere with exocytosis pathways mediated by the GTPase Rab11 and the exocyst complex. By doing so, anthrax or cholera toxins impair recycling of cadherins to cell-cell junctions and disrupt the barrier properties of endothelial cells or intestinal epithelial cells, respectively. Uropathogenic Escherichia coli (UPEC) is expelled from bladder epithelial cells through two different exocytic routes that involve sensing of bacteria in vacuoles by host Toll-like receptor 4 (TLR4) or monitoring of the pH of lysosomes harbouring UPEC. The TLR4 pathway is mediated by multiple Rab GTPases and the exocyst, whereas the other pathway involves exocytosis of lysosomes. Expulsion of UPEC through these pathways is thought to benefit the host.
许多微生物病原体共同利用或扰乱宿主膜运输途径。本综述涵盖了最近的一些例子,其中微生物与宿主胞吐作用相互作用,即细胞内囊泡与质膜融合。细菌病原体李斯特菌和金黄色葡萄球菌颠覆了胞吐作用的再循环内体途径,以诱导它们进入人体细胞。相比之下,原生动物病原体克氏锥虫或病毒腺病毒进入宿主细胞涉及溶酶体胞吐作用的利用。炭疽杆菌或霍乱弧菌产生的毒素干扰由 GTPase Rab11 和外泌体复合物介导的胞吐作用途径。通过这种方式,炭疽或霍乱毒素分别损害钙粘蛋白向细胞-细胞连接的再循环,并破坏内皮细胞或肠上皮细胞的屏障特性。尿路致病性大肠杆菌 (UPEC) 通过两种不同的胞吐途径从膀胱上皮细胞中排出,这两种途径涉及宿主 Toll 样受体 4 (TLR4) 对空泡中细菌的感应或对含有 UPEC 的溶酶体 pH 的监测。TLR4 途径由多种 Rab GTPase 和外泌体介导,而另一种途径涉及溶酶体的胞吐作用。认为通过这些途径排出 UPEC 有利于宿主。