Department of Medical Microbiology & Immunology, University of California at Davis, Davis, CA, USA.
Cell Microbiol. 2010 Sep 1;12(9):1195-202. doi: 10.1111/j.1462-5822.2010.01498.x. Epub 2010 Jul 28.
In humans, pathogenic Brucella species cause a febrile illness known as brucellosis. A key pathogenic trait of this group of organisms is their ability to survive in immune cells and persist in tissues of the reticuloendothelial system, a process that requires the function of a Type IV secretion system. In contrast to other well-studied Gram-negative bacteria, Brucella spp. do not cause inflammation at the site of invasion, but have a latency period of 2-4 weeks before the onset of symptoms. This review discusses several mechanisms that allow Brucella spp. both to evade detection by pattern recognition receptors of the innate immune system and suppress their signalling. In contrast to these stealth features, the VirB Type IV secretion system, which mediates survival within phagocytic cells, stimulates innate immune responses in vivo. The responses stimulated by this virulence factor are sufficient to check bacterial growth, but not to elicit sterilizing immunity. The result is a stand-off between host and pathogen that results in persistent infection.
在人类中，致病性布鲁氏菌会引起一种发热性疾病，称为布鲁氏菌病。该类生物体的一个关键致病特征是其能够在免疫细胞中存活并在网状内皮系统的组织中持续存在，这个过程需要 IV 型分泌系统的功能。与其他研究充分的革兰氏阴性菌不同，布鲁氏菌属不会在入侵部位引起炎症，而是在症状出现前有 2-4 周的潜伏期。这篇综述讨论了几种机制，这些机制使布鲁氏菌属既能逃避先天免疫系统模式识别受体的检测，又能抑制其信号转导。与这些隐身特征相反，VirB IV 型分泌系统介导吞噬细胞内的存活，在体内刺激先天免疫反应。该毒力因子刺激的反应足以抑制细菌生长，但不能引起杀菌性免疫。结果是宿主和病原体之间的僵持局面导致持续感染。
