Nassif X, So M
Institut National de la Santé et de la Recherche Medicale U411, Faculté de Médecine Necker-Enfants Malades, Université René Descartes, Paris, France.
Clin Microbiol Rev. 1995 Jul;8(3):376-88. doi: 10.1128/CMR.8.3.376.
The ability to interact with nonphagocytic cells is a crucial virulence attribute of the meningococcus and the genococcus. Like most bacterial pathogens, Neisseria meningitidis and Neisseria gonorrhoeae initiate infections by colonizing the mucosal epithelium, which serves as the site of entry. After this step, both bacteria cross the intact mucosal barrier. While N. gonorrhoeae is likely to remain in the subepithelial matrix, where it initiates an intense inflammatory reaction, N. meningitidis enters the bloodstream, and eventually the cerebrospinal fluid to cause meningitis. Both pathogens have evolved very similar mechanisms for interacting with host cells. Surface structures that influence bacterium-host interactions include pili, the meningococcal class 5 outer membrane proteins or the gonococcal opacity proteins, lipooligosaccharide, and the meningococcal capsule. This review examines what is known about the roles these structures play in bacterial adhesion and invasion, with special emphasis, on pilus-mediated adhesion. Finally, the importance of these structures in neisserial pathogenesis is discussed.
与非吞噬细胞相互作用的能力是脑膜炎奈瑟菌和淋病奈瑟菌的关键毒力属性。与大多数细菌病原体一样，脑膜炎奈瑟菌和淋病奈瑟菌通过定殖于作为进入部位的黏膜上皮来引发感染。在此步骤之后，两种细菌都会穿过完整的黏膜屏障。虽然淋病奈瑟菌可能会留在上皮下基质中，在那里引发强烈的炎症反应，但脑膜炎奈瑟菌会进入血液，最终进入脑脊液导致脑膜炎。两种病原体都进化出了非常相似的与宿主细胞相互作用的机制。影响细菌与宿主相互作用的表面结构包括菌毛、脑膜炎奈瑟菌5类外膜蛋白或淋病奈瑟菌不透明蛋白、脂寡糖和脑膜炎奈瑟菌荚膜。本综述探讨了这些结构在细菌黏附和侵袭中所起作用的已知情况，特别强调菌毛介导的黏附。最后，讨论了这些结构在奈瑟菌发病机制中的重要性。
