核苷酸结合寡聚化结构域样受体家族热蛋白结构域3炎性小体与牙周炎

摘要

核苷酸结合寡聚化结构域样受体家族热蛋白结构域(NLRP)3被激活后形成炎性小体,NLRP3炎性小体活化半胱氨酸天冬酰胺特异蛋白酶-1并进一步活化白细胞介素(IL)-1β前体,促进IL-1β释放以介导病原微生物的清除及相关程序性细胞死亡.IL-1β表达过量会造成牙髓炎、根尖周炎、牙周炎、牙槽骨丧失和口腔黏膜疾病的进一步发展.龈下菌斑与牙周炎密切相关,在龈下菌斑密度较高时,NLRP3炎性小体表达降低,炎性因子分泌减少,宿主对细菌的抵抗及清除力降低,有利于细菌的继续生存与定植.在根尖周炎和牙周炎的骨质破坏过程中,NLRP3炎性小体作为胞壁酰二肽及其分解产物的受体参与骨质吸收.调控NLRP3炎性小体及其下游炎性因子的表达,可能成为牙周炎治疗的方向之一.%Studies have shown that periodontitis has a certain relationship with nucleotide-binding oligomerization domain-like receptor family pyrin domain(NLRP)3 inflammasome.NLRP3 inflammasome plays an important role in the immune defense reaction of periodontal disease through regulating the release of interleukin(IL)-1β.NLRP3 inflammasome is comprised of NLRP3,apoptosis-associated speck-like protein,and cysteinyl aspartate-specific protease-1 and could promote the release of cytokines,thus removing pathogens and causing cell-related apoptosis.NLRP3 inflammasome is relevant with many oral diseases,such as chronic pulpitis and chronic apical periodontitis.This review will focus on NLRP3 inflammasome and its relevance with periodontitis.