炭疽与炎症小体。
Anthrax and the inflammasome.
机构信息
Laboratory of Bacterial Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Microbes Infect. 2012 May;14(5):392-400. doi: 10.1016/j.micinf.2011.12.005. Epub 2011 Dec 17.
Abstract
Anthrax lethal toxin (LT), a major virulence determinant of anthrax disease, induces vascular collapse in mice and rats. LT activates the Nlrp1 inflammasome in macrophages and dendritic cells, resulting in caspase-1 activation, IL-1β and IL-18 maturation and a rapid cell death (pyroptosis). This review presents the current understanding of LT-induced activation of Nlrp1 in cells and its consequences for toxin-mediated effects in rodent toxin and spore challenge models.
摘要
炭疽致死毒素 (LT) 是炭疽病的主要毒力决定因素，可导致小鼠和大鼠血管塌陷。LT 在巨噬细胞和树突状细胞中激活 Nlrp1 炎性体，导致 caspase-1 激活、IL-1β 和 IL-18 成熟以及细胞快速死亡（细胞焦亡）。本综述介绍了 LT 在细胞中诱导 Nlrp1 激活及其对啮齿动物毒素和孢子攻击模型中毒素介导效应的影响的最新认识。
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