Meyer T F
Max-Planck-Institut für Biologie, Abt. Infektionsbiologie, Tübingen.
Zentralbl Bakteriol. 1990 Nov;274(2):135-54. doi: 10.1016/s0934-8840(11)80098-8.
The outcome of the early stages of a neisserial infection is determined by receptor-mediated events that culminate in the attachment and invasion of human mucosal tissues. The factors participating in this process, including pili, opacity proteins (Opa), and perhaps lipopolysaccharide (LPS), are subject to complex genetic controls that allow these factors to be produced in multiple forms. Antigenic variation allows the pathogenic Neisseriae to evade the human immune response, and facilitates their interaction with a variety of different cells and tissues of the human host. One of the major genetic mechanisms causing antigenic variation is transformation, which allows virulence genes to be exchanged and recombined between independent Neisseria strains within multiply infected individuals. A number of other factors, such as IgA protease, alpha-factor, and the meningococcal capsule are also implicated in pathogenesis and render the pathogenic Neisseriae an excellent model for the investigation of bacterial virulence.
奈瑟菌感染早期阶段的结果取决于受体介导的一系列事件，这些事件最终导致人类黏膜组织的附着和侵袭。参与这一过程的因素，包括菌毛、不透明蛋白（Opa），或许还有脂多糖（LPS），受到复杂的基因控制，使得这些因素能够以多种形式产生。抗原变异使致病性奈瑟菌能够逃避人类免疫反应，并促进它们与人类宿主的多种不同细胞和组织相互作用。导致抗原变异的主要遗传机制之一是转化，它使毒力基因在多重感染个体内的独立奈瑟菌菌株之间进行交换和重组。许多其他因素，如IgA蛋白酶、α因子和脑膜炎球菌荚膜也与发病机制有关，使致病性奈瑟菌成为研究细菌毒力的理想模型。
