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

发布时间：2019-01-05 18:48

【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。
[Abstract]:Nucleotide binding oligodeoxynucleotide domain like receptor family (NLRP) 3 was activated to form inflammatory corpuscles. NLRP3 inflammatory corpuscles activated cysteine asparagine-specific protease 1 and further activated the precursor of interleukin (IL) 1 尾. To promote the release of IL-1 尾 to mediate the clearance of pathogenic microorganisms and related programmed cell death. Excessive expression of IL-1 尾 may lead to pulpitis, periapical periodontitis, alveolar bone loss and oral mucosal disease. Subgingival plaque is closely related to periodontitis. When the density of subgingival plaque is high, the expression of NLRP3 inflammatory corpuscles is decreased, the secretion of inflammatory factors is decreased, and the host resistance and clearance to bacteria are decreased, which is conducive to the survival and colonization of bacteria. In the process of bone destruction in periapical and periodontitis, NLRP3 inflammatory corpuscles are involved in bone resorption as receptors of cytosolic dipeptides and their decomposition products. Regulating the expression of NLRP3 inflammatory corpuscles and its downstream inflammatory factors may be one of the directions of periodontitis treatment.
【作者单位】：浙江大学医学院第二附属医院口腔科;
【基金】：国家自然科学基金(81271142,81400510)~~
【分类号】：R781.42

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