Institute of Biotechnology, Viikinkaari 1, University of Helsinki, FIN-00014, Helsinki, Finland.
Adv Exp Med Biol. 2011;715:1-15. doi: 10.1007/978-94-007-0940-9_1.
Bacteria of the Gram-negative genus Yersinia are environmentally ubiquitous. Three species are of medical importance: the intestinal pathogens Y. enterocolitica and Y. pseudotuberculosis, and the plague bacillus Y. pestis. The two former species, spread by contaminated food or water, cause a range of gastrointestinal symptoms and, rarely, sepsis. On occasion, the primary infection is followed by autoimmune sequelae such as reactive arthritis. Plague is a systemic disease with high mortality. It is a zoonosis spread by fleas, or more rarely by droplets from individuals suffering from pneumonic plague. Y. pestis is one of the most virulent of bacteria, and recent findings of antibiotic-resistant strains together with its potential use as a bioweapon have increased interest in the species. In addition to being significant pathogens in their own right, the yersiniae have been used as model systems for a number of aspects of pathogenicity. This chapter reviews the molecular mechanisms of adhesion in yersiniae. The enteropathogenic species share three adhesins: invasin, YadA and Ail. Invasin is the first adhesin required for enteric infection; it binds to β(1) integrins on microfold cells in the distal ileum, leading to the ingestion of the bacteria and allows them to cross the intestinal epithelium. YadA is the major adhesin in host tissues. It is a multifunctional protein, conferring adherence to cells and extracellular matrix components, serum and phagocytosis resistance, and the ability to autoagglutinate. Ail has a minor role in adhesion and serum resistance. Y. pestis lacks both invasin and YadA, but expresses several other adhesins. These include the pH 6 antigen and autotransporter adhesins. Also the plasminogen activator of Y. pestis can mediate adherence to host cells. Although the adhesins of the pathogenic yersiniae have been studied extensively, their exact roles in the biology of infection remain elusive.
革兰氏阴性耶尔森菌属的细菌在环境中无处不在。有三种医学上重要的物种：肠道病原体小肠结肠炎耶尔森菌和假结核耶尔森菌，以及鼠疫耶尔森菌。前两种物种通过受污染的食物或水传播，引起一系列胃肠道症状，很少引起败血症。偶尔，原发性感染会继发自身免疫性后遗症，如反应性关节炎。鼠疫是一种全身性疾病，死亡率很高。它是一种由跳蚤传播的动物传染病，或更罕见的是由患有肺鼠疫的个体飞沫传播。鼠疫耶尔森菌是最具毒性的细菌之一，最近发现的抗生素耐药菌株以及其作为生物武器的潜在用途增加了人们对该物种的兴趣。除了本身就是重要的病原体外，耶尔森氏菌还被用作致病性的许多方面的模型系统。本章综述了耶尔森氏菌的粘附分子机制。肠致病性种共享三种粘附素：侵袭素、YadA 和 Ail。侵袭素是肠感染所必需的第一个粘附素；它与回肠远端微褶皱细胞上的β(1)整合素结合，导致细菌被吞噬，并使它们穿过肠上皮。YadA 是宿主组织中的主要粘附素。它是一种多功能蛋白，赋予对细胞和细胞外基质成分、血清和吞噬作用的抵抗力以及自聚集的能力。Ail 在粘附和血清抗性中作用较小。鼠疫耶尔森氏菌缺乏侵袭素和 YadA，但表达其他几种粘附素。这些包括 pH6 抗原和自转运体粘附素。此外，鼠疫耶尔森氏菌的纤溶酶原激活剂也可以介导对宿主细胞的粘附。尽管致病性耶尔森氏菌的粘附素已经得到了广泛的研究，但它们在感染生物学中的确切作用仍不清楚。
