综述 Review

NOD1,NOD2和NLRP3炎症小体与牙髓炎

Published at: 2017年第37卷第4期

王雪纯 1 , 薛丽英 2
1 河北医科大学口腔医学院,石家庄 050011
2 河北医科大学病理学研究室,石家庄 050011
通讯作者 丽英 薛 Email: xueliying123@163.com
DOI: 10.3978/j.issn.2095-6959.2017.04.034
基金:

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(NOD like 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。


NOD1, NOD2 and NLRP3 inflammasome in pulpitis

Abstract

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. NOD1 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-1β, IL-6, IL-8 and IL-12. NLRP3 inflammasome activates caspase1 and mediates the release of IL-18 and IL-1β. 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 of pulpitis.


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引用

引用本文: 雪纯 王, 丽英 薛. NOD1,NOD2和NLRP3炎症小体与牙髓炎[J]. 临床与病理杂志, 2017, 37(4): 849-854.
Cite this article as: WANG Xuechun, XUE Liying . NOD1, NOD2 and NLRP3 inflammasome in pulpitis[J]. Journal of Clinical and Pathological Research, 2017, 37(4): 849-854.