Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS-induced septic shock

查看全文 作　　者：Kairui [1]Mao;Shuzhen [1]Chen;Mingkuan [2]Chen;Yonglei [2]Ma;Yan [2]Wang;Bo [3]Huang;Zhengyu [4]He;Yan [2]Zeng;Yu [1]Htl;Shuhui [5]Sun;Jing [6]Li;Xiaodong [1]Wu;Xiangrui [4]Wang;Warren [7]Strober;Chang [3]Chen;Guangxun [2]Meng;Bing [1,2]Sun

机构地区：[1]State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chi-nese Academy of Sciences, Shanghai 200031, China;[2]Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China;[3]National Labora-tory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beo'ing 100101, China;[4]Department of Anesthe-siology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, China Fudan University School of Medicine, Shanghai 200032, China; 6 Shanghai Information Center for Life Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; 7 Mucosal Immunity Section, Laboratory for Host Defenses, National In-stitute of Allergy and lnfectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA;[5]Fudan University School of Medicine, Shanghai 200032, China;[6]Shanghai Information Center for Life Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;[7]Mucosal Immunity Section, Laboratory for Host Defenses, National In-stitute of Allergy and lnfectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA

出　　处：《Cell Research》索引2013年第23卷第2期,共12页

基　　金：We thank R Caspi (National Eye Institute, NIH, USA) and D Li (Shanghai Institutes for Biological Sciences, China) for helpful comments, and S Skinner for critical reading of the manuscript. This work was supported by the National Basic Research Program of China (973 program, 2013CB530504), the National Natural Science Foundation of China (31230024, 31030029, 31100662, 31030023, 91029707, 31170868), the Shanghai Natural Science Foundation (11ZR1442600), the National Ministry of Science and Technology (2007DFC31700), the National Science and Technology Major Project (2008ZX10004-002, 2008ZX10002-014, 2009ZX10004-105, 2009ZXI0004-016, 2011ZX10004-001 and 2012ZXl0002007), the Shanghai Pasteur Health Research Foundation (SPHRF2008001 and SPHRF2009001), the SA-SIBS Discovery Innovation Grant, the Li Kha Shing Foundation and the 100 Talent Program of the Chinese Academy of Sciences (to GM). 摘　　要：Inflammasomes 是触发 caspase-1 的激活和 interleukin-1β 的成熟的多蛋白质建筑群;(IL-1β) ,然而,这些建筑群的规定仍然保持糟糕描绘了。这里,我们显示出那氮的氧化物(没有) 禁止了调停 NLRP3 的 ASC pyroptosome 形成, caspase-1 激活和 IL-1β在从老鼠和人的 myeloid 房间的分泌物。同时,内长不否定地也源于 iNOS (没有 synthase 的可诱导的形式) 调整 NLRP3 inflammasome 激活。iNOS 的弄空响应 LPS 和 ATP 导致了不正常的线粒体的增加的累积,它为增加的 IL-1β 负责;生产和 caspase-1 激活。没有生产的 iNOS 缺乏或药理学抑制在 vivo 提高了 NLRP3 依赖的 cytokine 生产,因此在老鼠从导致 LPS 的败血增加死亡,它被 NLRP3 阻止缺乏。我们的结果因此经由线粒体的稳定作为 NLRP3 inflammasome 的一个批评否定管理者不识别。这研究有重要含意让新策略的设计控制 NLRP3 相关的疾病。 关键词：诱导型一氧化氮合酶 LPS 感染性休克激活白细胞介素-1 iNOS 负调控因子保护

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Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS-induced septic shock

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