Innate immunity against Francisella tularensis is dependent on the ASC/caspase-1 axis.
Innate immunity against Francisella tularensis is dependent on the ASC/caspase-1 axis.
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DOI：
10.1084/jem.20050977
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发表时间：
2005-10-17
期刊：
影响因子：
--
通讯作者：
Monack DM
中科院分区：
文献类型：
--
作者：
Mariathasan S;Weiss DS;Dixit VM;Monack DM
土拉热弗朗西丝菌是一种引起人畜共患土拉菌病的革兰氏阴性球杆菌。这种细菌病原体在暴露于10个细胞后会导致人类患上一种类似狂犬病的疾病。先天免疫系统对抗弗朗西斯菌的许多机制尚不清楚。在这里，我们表明，野生型弗朗西斯，达到胞质溶胶，但不是弗朗西斯突变体，仍然定位于液泡，诱导宿主防御反应的巨噬细胞，这是依赖于caspase-1和死亡倍含有衔接蛋白ASC。Caspase-1和ASC信号传导导致宿主细胞死亡和促炎细胞因子白细胞介素（IL）-1β和IL-18的释放。F.与野生型小鼠相比，土拉热感染的胱天蛋白酶-1和ASC缺陷型小鼠显示出显著增加的细菌负荷和死亡率，证明胱天蛋白酶-1和ASC在对抗该病原体感染的先天防御中起关键作用。
Francisella tularensis is a highly infectious gram-negative coccobacillus that causes the zoonosis tularemia. This bacterial pathogen causes a plague-like disease in humans after exposure to as few as 10 cells. Many of the mechanisms by which the innate immune system fights Francisella are unknown. Here we show that wild-type Francisella, which reach the cytosol, but not Francisella mutants that remain localized to the vacuole, induced a host defense response in macrophages, which is dependent on caspase-1 and the death-fold containing adaptor protein ASC. Caspase-1 and ASC signaling resulted in host cell death and the release of the proinflammatory cytokines interleukin (IL)-1β and IL-18. F. tularensis–infected caspase-1– and ASC-deficient mice showed markedly increased bacterial burdens and mortality as compared with wild-type mice, demonstrating a key role for caspase-1 and ASC in innate defense against infection by this pathogen.
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