NOD1，NOD2和NLRP3炎症小体与牙髓炎
| 作者: |
1王雪纯,
2薛丽英
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: |
薛丽英
Email: xueliying123@163.com |
| DOI: | 10.3978/j.issn.2095-6959.2017.04.034 |
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。
关键词：
NOD1
NOD2
NLRP3炎症小体
牙髓炎
固有免疫
NOD1, NOD2 and NLRP3 inflammasome in pulpitis
CorrespondingAuthor: XUE Liying Email: xueliying123@163.com
DOI: 10.3978/j.issn.2095-6959.2017.04.034
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.