慢性感染会通过NLRP3炎性体引起有害促炎细胞因子——白细胞介素1(IL-1)的产生。来自美国麻省大学医学院的Sassetti等研究人员发现当一氧化氮(NO)分子附加到NLRP3时,NLRP3炎性体的组装受抑制。这种通过炎症体的亚硝酰化调控炎症的机制,在限制抗感染过程中产生的附带伤害方面或将重要的作用。相关的研究论文于2012年11月18日在线发表在《Nature Immunology》杂志上。

-2013年1月《自然-免疫》

中文翻译


【题目】NO通过抑制NLRP3炎性体依赖的IL-1β加工过程控制结核病

【译文】白细胞介素(IL-1)是先天免疫的重要中介物,但也能造成炎症性组织损伤。在结核病中,如慢性感染病,IL-1的有益抗菌作用必须与预防免疫病理学的需要相平衡。通过外部手段控制活体内结核分支杆菌(Mycobacterium tuberculosis)的繁殖,本研究排除了抗菌免疫的因素,同时发现淋巴细胞分泌的干扰素γ(IFN-γ)能够抑制IL-1的产生和感染诱导的免疫病理症状。这些效应是由一氧化氮(NO)调控,本研究发现NO能通过硫醇亚硝基化作用特异性抑制NLRP3炎性体的组装。本研究结果表明NO的产生是适应性免疫的结果,NO是调节由持续性感染引起的破坏性先天免疫响应所不可缺少的。

英文原稿


[Title]: Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome–dependent processing of IL-1β 

[Authors]:Bibhuti B Mishra, Vijay A K Rathinam, Gregory W Martens, Amanda J Martinot, Hardy Kornfeld, Katherine A Fitzgerald & Christopher M Sassetti

[Abstract]: Interleukin 1 (IL-1) is an important mediator of innate immunity but can also promote inflammatory tissue damage. During chronic infections such as tuberculosis, the beneficial antimicrobial role of IL-1 must be balanced with the need to prevent immunopathology. By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, we obviated the requirement for antimicrobial immunity and discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ). This effect was mediated by nitric oxide (NO), which we found specifically inhibited assembly of the NLRP3 inflammasome via thiol nitrosylation. Our data indicate that the NO produced as a result of adaptive immunity is indispensable in modulating the destructive innate inflammatory responses elicited during persistent infections.

原文地址

http://www.nature.com/ni/journal/v14/n1/full/ni.2474.html

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1 条回复 » to “《Nature Immunology》2013.01-NO通过抑制NLRP3炎性体依赖的IL-1β加工过程控制结核病”

  1. hyl 说道:

    很好研究结果!

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