Type I interferon signaling is required for activation of the inflammasome during Francisella infection.
Type I interferon signaling is required for activation of the inflammasome during Francisella infection.
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I型干扰素信号在弗朗西斯拉感染过程中激活炎症体需要。
DOI：
10.1084/jem.20062665
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发表时间：
2007-05-14
影响因子：
15.3
通讯作者：
Monack, Denise M.
中科院分区：
文献类型：
--
作者：
Henry, Thomas;Brotcke, Anna;Weiss, David S.;Thompson, Lucinda J.;Monack, Denise M.
土拉热弗朗西丝菌是一种致病性细菌，其毒力与其在宿主细胞胞质溶胶内复制的能力有关。进入巨噬细胞胞质溶胶激活称为炎性体的宿主保护性多分子复合物，释放促炎细胞因子白介素（IL）-1β和-18，并触发caspase-1依赖性细胞死亡。在这项研究中，我们表明，胞质F。tularensis novicida（F. novicida）诱导I型干扰素（IFN）应答，该应答对于胱天蛋白酶-1活化、炎性小体介导的细胞死亡以及IL-1β和IL-18的释放是必需的。在F.杀线虫感染。I型IFN也是响应于胞质单核细胞增生李斯特菌而不是空泡定位的沙门氏菌肠血清型鼠伤寒沙门氏菌或细胞外三磷酸腺苷的炎性体活化所必需的。这些结果显示了I型IFN信号传导和炎性小体激活之间的特异性联系，这是由胞质细菌识别触发的两个连续事件。据我们所知，这是第一个炎性小体激活正调控的例子。这种联系强调了病原体的胞质识别的重要性，并突出了多个先天免疫途径如何相互作用之前承诺的关键主机响应。
Francisella tularensis is a pathogenic bacterium whose virulence is linked to its ability to replicate within the host cell cytosol. Entry into the macrophage cytosol activates a host-protective multimolecular complex called the inflammasome to release the proinflammatory cytokines interleukin (IL)-1β and -18 and trigger caspase-1–dependent cell death. In this study, we show that cytosolic F. tularensis subspecies novicida (F. novicida) induces a type I interferon (IFN) response that is essential for caspase-1 activation, inflammasome-mediated cell death, and release of IL-1β and -18. Extensive type I IFN–dependent cell death resulting in macrophage depletion occurs in vivo during F. novicida infection. Type I IFN is also necessary for inflammasome activation in response to cytosolic Listeria monocytogenes but not vacuole-localized Salmonella enterica serovar Typhimurium or extracellular adenosine triphosphate. These results show the specific connection between type I IFN signaling and inflammasome activation, which are two sequential events triggered by the recognition of cytosolic bacteria. To our knowledge, this is the first example of the positive regulation of inflammasome activation. This connection underscores the importance of the cytosolic recognition of pathogens and highlights how multiple innate immunity pathways interact before commitment to critical host responses.
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影响因子：
16
作者：
Martinon, F;Burns, K;Tschopp, J
通讯作者：
Tschopp, J
DOI：
10.1073/pnas.0504271103
发表时间：
2006-01-03
影响因子：
11.1
作者：
Gavrilin, MA;Bouakl, IJ;Wewers, MD
通讯作者：
Wewers, MD
DOI：
10.1084/jem.20050977
发表时间：
2005-10-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Mariathasan S;Weiss DS;Dixit VM;Monack DM
通讯作者：
Monack DM
DOI：
10.1073/pnas.0601838103
发表时间：
2006-09-26
影响因子：
11.1
作者：
Checroun, Claire;Wehrly, Tara D.;Celli, Jean
通讯作者：
Celli, Jean
DOI：
10.1073/pnas.96.5.2396
发表时间：
1999-03-02
影响因子：
11.1
作者：
Hersh, D;Monack, DM;Zychlinsky, A
通讯作者：
Zychlinsky, A