NOD1,NOD2和NLRP3炎症小体与牙髓炎

摘要

模式识别受体(pattern recognition receptors,PRRs)识别病原相关分子模式(pathogen associated molecule patterns,PAMP)激活固有免疫系统,是抵抗病原微生物入侵的第一道防线.核苷酸结合寡聚化结构域蛋白(nucleotide-binding oligomerization domains,NODs)和NOD样受体蛋白3(NODlike protein 3,NLRP3)属胞质内PRRs家族.NOD1和NOD2激活NF-κB,MAPK,JNK,p38和ERK信号通路,促进TNF-α,IL-1β,IL-6,IL-8和IL-12等多种炎性因子的转录表达.NLRP3炎症小体激活caspase-1,并促进IL-18和IL-1β表达.牙髓位于低顺应性根管系统中,牙髓环境环境与机体其他组织不同.目前的研究表明NOD1,NOD2和NLRP3炎症小体与牙髓固有免疫及牙髓炎的发生、发展有关.%Pathogen associated molecule patterns (PAMPs) recognition by pattern recognition receptors (PRRs) activates the initiation of innate immunity,which plays a key role in first-line defense.Nucleotide-binding oligomerization domains (NODs) and NOD like protein 3 (NLRP3) are a group of evolutionarily conserved intracellular PRRs.NOD 1 and NOD2 activates NF-κB,MAPK,JNK,p38 and ERK signaling pathways and stimulates the expression of various inflammatory factors,such as TNF-α,IL-1 β,IL-6,IL-8 and IL-12.NLRP3 inflammasome activates caspase 1 and mediates the release of IL-18 and IL-1 β.The environment of the dental pulp is substantially different from that of other tissues of the body,which resides in a low compliance root canal system.Accumulated data indicate that NOD1,NOD2 and NLRP3 play a key role in the innate immunity of pulp and modulatory effect in the immune defense responses during the progression ofpulpitis.