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Cell Reports:中国研究发现手足口病毒免疫调控新机制

2015-07-17 佚名 上海巴斯德所

6月24日,国际学术期刊Cell Reports在线发表了中国科学院上海巴斯德研究所孟广勋课题组和中国医学科学院病原生物学研究所王健伟课题组合作的最新科研成果“Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome”(肠道病毒71型与NLRP3炎症小体的相互调控作用研究)。该研究首次发现了重要天然免疫分子NLR

6月24日,国际学术期刊Cell Reports在线发表了中国科学院上海巴斯德研究所孟广勋课题组和中国医学科学院病原生物学研究所王健伟课题组合作的最新科研成果“Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome”(肠道病毒71型与NLRP3炎症小体的相互调控作用研究)。该研究首次发现了重要天然免疫分子NLRP3在肠道病毒71型(EV71)感染中的保护作用以及EV71通过其编码的蛋白酶切割NLRP3的互作机制。 
  
肠道病毒71型(EV71)是手足口病的主要致病原,主要感染对象为婴儿和低龄儿童,感染后可引起肺水肿和脑炎等并发症,严重危害婴幼儿生命健康。目前,对于EV71感染的致病机制和宿主免疫反应机制的研究较为缺乏。 
  
NLRP3炎症小体是以NLRP3、ASC、Caspase-1为核心蛋白组成的大分子复合体,主要功能是识别外源感染和内部损伤等危险信号,诱导多效性细胞因子IL-1b和IL-18的分泌。NLRP3炎症小体广泛参与多种病原体的识别,但其在EV71感染过程中的作用尚不清楚。 
  
上海巴斯德研究所天然免疫课题组研究生王洪斌、中国医学科学院病原生物学研究所雷晓波博士等在孟广勋研究员和王健伟研究员的指导下,发现了NLRP3炎症小体缺失的小鼠感染EV71后疾病程度明显比野生型小鼠严重,说明NLRP3炎症小体在EV71感染过程中对小鼠具有保护作用;体外实验也证明了EV71能够在髓系细胞上激活NLRP3炎症小体并诱导IL-1b 分泌。此外,EV71在激活NLRP3炎症小体的同时,也能通过其编码的蛋白酶2A和3C切割NLRP3来抑制炎症小体的激活。该项研究成果揭示了EV71与NLRP3炎症小体的对抗调控机制,并为抗病毒治疗提供了新的参考靶标。 
    
该研究得到了上海巴斯德研究所冷启彬研究员和黄忠研究员的协助,并获得了国家自然科学基金委面上项目、重大研究计划项目,科技部973项目,国家科技重大专项等经费支持。



图1.  A,3日龄WT、Nlrp3-/-、Asc-/-和Caspase1-/-小鼠颅内注射EV71后,连续15天小鼠的疾病程度曲线. B,THP-1细胞在用不同浓度病毒、不同时间感染后,细胞上清中IL-1β的含量. C,293细胞中共表达NLRP3与EV71病毒蛋白2A、2A突变体(C110A)、3C或3C突变体(C147S)后通过western blot检测被切割的NLRP3.
 


图2.  EV71在髓系细胞中的复制激活NLRP3炎症小体;EV71也能通过其编码的蛋白酶2A和3C切割NLRP3,从而抑制NLRP3炎症小体的激活。

原始出处:

Hongbin Wang, Xiaobo Lei, Xia Xiao,et al.Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome.Cell Reperts.Volume 12, Issue 1, p42–48, 7 July 2015

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    2016-04-21 lingqf
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    2015-08-23 智智灵药
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    2015-07-22 1dd81045m14(暂无匿称)

    厉害

    0

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