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中国科大破解炎症发生机制

2017-08-11 12:14:18   国际在线

慢性炎症反应参与几乎所有人类重大疾病的发生过程,因此了解炎症反应的发生过程有可能为疾病治疗提供新的策略。近日出版的《自然·通讯》杂志上,一项研究成果揭示了胞内氯离子通道蛋白CLICs家族在NLRP3炎症小体活化中的重要作用。

该项研究成果由中国科学技术大学生命科学学院、微尺度国家实验室及中科院天然免疫和慢性疾病重点实验室周荣斌、江维教授研究组与王均教授研究组、白丽教授研究组及中山大学崔隽教授研究组合作完成。

NLRP3炎症小体作为一种多蛋白复合物,其活化能够促进IL-1b和IL-18等促炎因子的成熟和分泌,从而促进炎症反应的发生过程。近年来,NLRP3炎症小体被报道参与2型糖尿病、痛风、帕金森等多种重大疾病的发生过程,探究NLRP3炎症小体的活化机制,能提供潜在的治疗手段。

NLRP3炎症小体能够感知机体内外多种危险信号,比如高血糖、高血脂、尿酸结晶、胆固醇结晶等,但是上述危险信号诱导NLRP3活化的分子机制还很不清楚。过去的研究工作表明,危险信号可以诱导胞内钾离子的流失和线粒体损伤,但是胞内钾离子变化和线粒体损伤如何诱发后续炎症小体组装的分子机制尚未被揭示。

此次研究工作发现,CLICs蛋白家族在线粒体损伤产生的活性氧的诱导下能够迁移到细胞膜上,介导胞内氯离子的外流,从而进一步促进NLRP3炎症小体的组装,抑制CLICs家族蛋白的表达或者活性能够显著抑制NLRP3炎症小体活化。该项工作不仅发现CLICs介导的氯离子外流是NLRP3炎症小体组装上游的一个关键时间,还提示可以靶向CLICs缓解NLRP3相关的炎症性疾病。(记者吴长锋)

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