NLRP3炎症小体调节创伤后炎症反应的作用

摘要

创伤在造成机体原发损伤的同时,诱发炎症反应,对机体产生继发性损伤.炎症小体通过影响促炎细胞因子的裂解及其成熟、释放来调节炎症反应.NLRP3炎症小体能活化半胱氨酸天冬氨酸酶-1(Caspase-1),并引起白细胞介素(IL-1β、IL-18)等促炎细胞因子的分泌,参与机体抵抗病原体的免疫应答.本文就NLRP3炎症小体在创伤诱发的炎症反应中的作用的研究进展做一综述.%Trauma can not only cause primary damage to the injured body, but also result in the secondary dam-nification to the same body by inducing the inflammatory response. The inflammasome can regulate inflammation by in-fluencing the lysis and releases of proinflammatory cytokines. The NOD-, LRR, and pyrin domain-containing 3 (NL-RP3) inflammasome activates the cysteine aspartase-1 (Caspase-1), causes the secretion of proinflammatory cytokines, such as interleukin (IL-1β, and IL-18), which involved in the immune response to resist pathogens in the body. Here we review the role of the NLRP3 inflammasome in inflammation after injury.