摘要
真核细胞能够启动多种不同的自杀程序,非炎性的和促炎性的细胞死亡程序均可引起细胞应答,从而导致重要系统生理反应的发生。焦亡是一种由caspase-1依赖性介导的新的促炎程序性细胞死亡方式,伴有大量促炎因子的释放并诱发级联放大的炎症反应,对控制微生物感染非常关键。在不断的进化过程中,病原体为增强自身引发疾病的能力出现了抑制焦亡的机制,即通过宿主细胞和病原体的竞争关系控制焦亡的发生,竞争结果可直接影响宿主细胞内炎症的爆发甚至细胞的存亡。论文对细胞焦亡的机制和特征、NLRs与炎症小体、炎症因子的形成和分泌的研究进展进行了综述,以期为炎症机制的研究提供参考。
Several distinct programmes of self-destruction can be initiated by eukaryotic cells, and non-in-flammatory or proinflammatory cell death process can instruct responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis is a new way of inflammatory pro-grammed cell death,which is mediated by caspase-1 and accompanied by the release of a large amount of proinflammatory factor and inducing a cascade amplification of the inflammatory response. It is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis and enhance their ability to persist and cause disease. There is a competition between host and pathogen to regulate pyropto-sis, and the outcome immediately impacts inflammation and life or death of the host. The mechanism and characteristics of pyroptosis and research progress of NLRs and inflammasome, formation and secretion of inflammatory cytokines were reviewed in this paper, so as to provide reference for the study of inflammato-ry mechanism.
出处
《动物医学进展》
北大核心
2017年第9期101-104,共4页
Progress In Veterinary Medicine
基金
国家自然科学基金项目(31660704)
云南省教育厅科学研究基金项目(2017YJS028)
