国际口腔医学杂志

国际口腔医学杂志 ›› 2017, Vol. 44 ›› Issue (4): 484-487.doi: 10.7518/gjkq.2017.04.022

• 综述 • 上一篇    下一篇

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

王娜娜, 陈莉丽, 丁佩惠   

  1. 浙江大学医学院第二附属医院口腔科 杭州 310006
  • 收稿日期:2016-09-01 修回日期:2017-02-22 出版日期:2017-07-01 发布日期:2017-07-01
  • 通讯作者: 丁佩惠,教授,博士,Email：phding@163.com
  • 作者简介:王娜娜,硕士,Email：nana_199210@163.com
  • 基金资助:
    国家自然科学基金（81271142,81400510）

Nucleotide-binding oligomerization domain-like-receptor family pyrin domain 3 inflammasome and periodontitis

Wang Nana, Chen Lili, Ding Peihui   

  1. Dept. of Stomatology, The Affiliated Second Hospital of Medical School, Zhejiang University, Hangzhou 310006, China
  • Received:2016-09-01 Revised:2017-02-22 Online:2017-07-01 Published:2017-07-01
  • Supported by:
    This study was supported by the National Natural Science Foundation of China(81271142, 81400510).

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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。

关键词: 牙周炎, 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, 白细胞介素

Abstract: 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.

Key words: periodontitis, nucleotide-binding oligomerization domain-like-receptor family pyrin domain 3 inflammasome, interleukin

中图分类号: 

  • R781.4+2
[1] Kebschull M, Demmer RT, Papapanou PN. “Gum bug, leave my heart alone!”—epidemiologic and mechanistic evidence linking periodontal infections and atherosclerosis[J]. J Dent Res, 2010, 89(9):879- 902.
[2] Madianos PN, Bobetsis YA, Offenbacher S. Adverse pregnancy outcomes(APOs) and periodontal disease: pathogenic mechanisms[J]. J Periodontol, 2013, 84(4 Suppl):S170-S180.
[3] Janssen KM, Vissink A, de Smit MJ, et al. Lessons to be learned from periodontitis[J]. Curr Opin Rheu-matol, 2013, 25(2):241-247.
[4] Franchi L, Eigenbrod T, Muñoz-Planillo R, et al. The inflammasome: a caspase-1-activation platform that regulates immune responses and disease patho-genesis[J]. Nat Immunol, 2009, 10(3):241-247.
[5] Schroder K, Tschopp J. The inflammasomes[J]. Cell, 2010, 140(6):821-832.
[6] Mariathasan S, Weiss DS, Newton K, et al. Cryop-yrin activates the inflammasome in response to to-xins and ATP[J]. Nature, 2006, 440(7081):228-232.
[7] Dinarello CA. Immunological and inflammatory functions of the interleukin-1 family[J]. Annu Rev Immunol, 2009, 27:519-550.
[8] Hoffman HM, Wanderer AA. Inflammasome and IL-1beta-mediated disorders[J]. Curr Allergy Asthma Rep, 2010, 10(4):229-235.
[9] Kanneganti TD, Özören N, Body-Malapel M, et al. Bacterial RNA and small antiviral compounds ac-tivate caspase-1 through cryopyrin/Nalp3[J]. Nature, 2006(7081):233-236.
[10] Song-Zhao GX, Srinivasan N, Pott J, et al. Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen[J]. Mucosal Immunol, 2014, 7 (4):763-774.
[11] Rehaume LM, Jouault T, Chamaillard M. Lessons from the inflammasome: a molecular sentry linking Candida and Crohn’s disease[J]. Trends Immunol, 2010, 31(5):171-175.
[12] Zaki MH, Boyd KL, Vogel P, et al. The NLRP3 in-flammasome protects against loss of epithelial in-tegrity and mortality during experimental colitis[J]. Immunity, 2010, 32(3):379-391.
[13] Kummer JA, Broekhuizen R, Everett H, et al. In-flammasome components NALP 1 and 3 show dis-tinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response[J]. J Histochem Cytochem, 2007, 55(5): 443-452.
[14] Belibasakis GN, Meier A, Guggenheim B, et al. Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells[J]. Mic-rob Pathog, 2011, 50(1):6-11.
[15] Brandtzaeg P. Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses [J]. Acta Odontol Scand, 2001, 59(4):235-243.
[16] Darveau RP, Hajishengallis G, Curtis MA. Porphy-romonas gingivalis as a potential community activist for disease[J]. J Dent Res, 2012, 91(9):816-820.
[17] Bostanci N, Emingil G, Saygan B, et al. Expression and regulation of the NALP3 inflammasome com-plex in periodontal diseases[J]. Clin Exp Immunol, 2009, 157(3):415-422.
[18] Park E, Na HS, Song YR, et al. Activation of NLRP3 and AIM2 inflammasomes by Porphyromonas gin-givalis infection[J]. Infect Immun, 2014, 82(1):112- 123.
[19] Gamonal J, Acevedo A, Bascones A, et al. Levels of interleukin-1β, -8, and -10 and RANTES in gingival crevicular fluid and cell populations in adult perio-dontitis patients and the effect of periodontal treat-ment[J]. J Periodontol, 2000, 71(10):1535-1545.
[20] Yilmaz O, Sater AA, Yao L, et al. ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by Porphyromonas gingivalis [J]. Cell Microbiol, 2010, 12(2):188-198.
[21] Bostanci N, Meier A, Guggenheim B, et al. Regula-tion of NLRP3 and AIM2 inflammasome gene ex-pression levels in gingival fibroblasts by oral bio-films[J]. Cell Immunol, 2011, 270(1):88-93.
[22] Safavi KE, Nichols FC. Effects of a bacterial cell wall fragment on monocyte inflammatory function [J]. J Endod, 2000, 26(3):153-155.
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