国际口腔医学杂志 ›› 2017, Vol. 44 ›› Issue (6): 660-663.doi: 10.7518/gjkq.2017.06.007

• 牙周专栏 • 上一篇    下一篇

细胞焦亡与牙龈卟啉单胞菌的关系及其在牙周病发生发展中的作用机制

唐秋玲, 李格格, 潘佳慧, 侯玉帛, 孟阳, 于维先   

  1. 吉林大学口腔医院牙周病科,吉林省牙发育及颌骨重塑与再生重点实验室 长春 130021
  • 收稿日期:2017-02-07 修回日期:2017-07-15 出版日期:2017-11-01 发布日期:2017-11-01
  • 通讯作者: 于维先,教授,博士,Email:yu-wei-xian@163.com
  • 作者简介:唐秋玲,硕士,Email:1099524983@qq.com
  • 基金资助:
    国家自然科学基金面上项目(81570983); 吉林省科技厅自然科学基金项目(20150101076JC)

Mechanism of pyroptosis and Porphyromonas gingivalis in periodontitis development process

Tang Qiuling, Li Gege, Pan Jiahui, Hou Yubo, Meng Yang, Yu Weixian.   

  1. Dept. of Periodontology, School and Hospital of Stomatology, Jilin University;Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun 130021, China
  • Received:2017-02-07 Revised:2017-07-15 Online:2017-11-01 Published:2017-11-01
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81570983) and Natural Science Foundation of Science and Technology Department of Jilin Province(20150101076JC).

摘要: 细胞焦亡是一种典型的程序性细胞死亡方式,主要通过炎症小体的介导,并伴有大量促炎性细胞因子的释放。牙龈卟啉单胞菌作为牙周炎的关键致病菌,一方面可通过激活牙周组织中巨噬细胞内核苷酸结合寡聚化结构域样受体蛋白3炎症小体,促进细胞焦亡,引发牙周组织免疫病理损伤;另一方面,牙龈卟啉单胞菌通过抑制血管内皮细胞焦亡,逃逸免疫系统的杀伤作用,促进自身生存。本文就细胞焦亡及其在牙周炎中的作用机制作一综述。

关键词: 牙周炎, 细胞焦亡, 作用机制

Abstract: Pyroptosis is a typical form of programmed cell death mediated by inflammasomes. It leads to inflammatory response through the release of pro-inflammatory cytokines. Porphyromonas gingivalis is the keystone pathogen of periodontitis. On the one hand, it can activate thenucleotide-binding oligomerization domain like receptor protein 3 inflammasomes of macrophages in the periodontal tissue, and it also can promote pyroptosis that lead to the immune pathological damage of periodontal tissue; on the other hand, it restrain the pyroptosis of vascular endothelial cell and escape the killing of the immune system. In this paper, the recent progress and mechanism of pyroptosis in periodontitis are reviewed.

Key words: periodontitis, pyroptosis, mechanism

中图分类号: 

  • R781.4
[1] Ghonime MG, Shamaa OR, Eldomany RA, et al. Tyro-sine phosphatase inhibition induces an ASC-depen-dent pyroptosis[J]. Biochem Biophys Res Commun, 2012, 425(2):384-389.
[2] Bostanci N, Emingil G, Saygan B, et al. Expression and regulation of the NALP3 inflammasome complex in periodontal diseases[J]. Clin Exp Immunol, 2009, 157(3):415-422.
[3] Blander JM. A long-awaited merger of the pathways mediating host defence and programmed cell death [J]. Nat Rev Immunol, 2014, 14(9):601-618.
[4] Galluzzi L, Vitale I, Abrams JM, et al. Molecular definitions of cell death subroutines: recommenda-tions of the Nomenclature Committee on Cell Death 2012[J]. Cell Death Differ, 2012, 19(1):107-120.
[5] Shi JJ, Zhao YE, Wang K, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015, 526(7575):660-665.
[6] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44.
[7] Broz P. Immunology: caspase target drives pyroptosis [J]. Nature, 2015, 526(7575):642-643.
[8] Lim Y, Kumar S. A single cut to pyroptosis[J]. Onco-target, 2015, 6(35):36926-36927.
[9] He WT, Wan H, Hu L, et al. Gasdermin D is an exe-cutor of pyroptosis and required for interleukin-1β secretion[J]. Cell Res, 2015, 25(12):1285-1298.
[10] Genco RJ, Van Dyke TE. Prevention: reducing the risk of CVD in patients with periodontitis[J]. Nat Rev Cardiol, 2010, 7(9):479-480.
[11] Takahashi Y, Davey M, Yumoto H, et al. Fimbria-dependent activation of pro-inflammatory molecules in Porphyromonas gingivalis infected human aortic endothelial cells[J]. Cell Microbiol, 2006, 8(5):738- 757.
[12] Kataoka H, Kono H, Patel Z, et al. Evaluation of the contribution of multiple DAMPs and DAMP recep-tors in cell death-induced sterile inflammatory res-ponses[J]. PLoS One, 2014, 9(8):e104741.
[13] Ito Y, Bhawal UK, Sasahira T, et al. Involvement of HMGB1 and RAGE in IL-1β-induced gingival infla-mmation[J]. Arch Oral Biol, 2012, 57(1):73-80.
[14] Li G, Liang X, Lotze MT. HMGB1: the central cyto-kine for all lymphoid cells[J]. Front Immunol, 2013, 4(4):68.
[15] Andersson U, Tracey KJ. HMGB1 is a therapeutic target for sterile inflammation and infection[J]. Annu Rev Immunol, 2011, 29:139-162.
[16] Di Benedetto A, Gigante I, Colucci S, et al. Perio-dontal disease: linking the primary inflammation to bone loss[J]. Clin Dev Immunol, 2013, 2013:503754.
[17] Chakraborty R, Bhatt KH, Sodhi A. High mobility group box 1 protein synergizes with lipopolysacc-haride and peptidoglycan for nitric oxide production in mouse peritoneal macrophages in vitro [J]. Mol Immunol, 2013, 54(1):48-57.
[18] Man SM, Kanneganti TD. Gasdermin D: the long-awaited executioner of pyroptosis[J]. Cell Res, 2015, 25(11):1183-1184.
[19] Schroder K, Tschopp J. The inflammasones[J]. Cell, 2010, 140(6):821-832.
[20] Shi JJ, Zhao YE, Wang YP, et al. Inflammatory cas-pases are innate immune receptors for intracellular LPS[J]. Nature, 2014, 514(7521):187.
[21] Suzuki T, Franchi L, Toma C, et al. Differential regulation of caspase-1 activation, pyroptosis, and autophagy via Ipaf and ASC in Shigella -infected macrophages[J]. PLoS Pathog, 2007, 3(8):e111.
[22] Benedyk M, Mydel PM, Delaleu N, et al. Gingipains: critical factors in the development of aspiration pne-umonia caused by Porphyromonas gingivalis [J]. J Innate Immun, 2016, 8(2):185-198.
[23] Lausson S, Cressent M. Signal transduction pathways mediating the effect of adrenomedullin on osteoblast survival[J]. J Cell Biochem, 2011, 112(12):3807- 3815.
[24] 陈玉婷, 宋祥晨, 张福萍, 等. 促凋亡蛋白Bim、Bax和Bak在牙龈蛋白酶诱导成骨细胞凋亡中的表达[J]. 中华口腔医学杂志, 2013, 48(5):272-277.
Chen YT, Song XC, Zhang FP, et al. Expression of Bim, Bax and Bak in the process of gingipain-induced osteoblast apoptosis[J]. Chin J Stomatol, 2013, 48 (5):272-277.
[25] Huang MT, Taxman DJ, Holley-Guthrie EA, et al. Critical role of apoptotic speck protein containing a caspase recruitment domain(ASC) and NLRP3 in causing necrosis and ASC speck formation induced by Porphyromonas gingivalis in human cells[J]. J Immunol, 2009, 182(4):2395-2404.
[26] Kolev M, Le Friec G, Kemper C. Complement—tap-ping into new sites and effector systems[J]. Nat Rev Immunol, 2014, 14(12):811-820.
[27] Maekawa T, Krauss JL, Abe T, et al. Porphyromonas gingivalis manipulates complement and TLR signa-ling to uncouple bacterial clearance from inflamma-tion and promote dysbiosis[J]. Cell Host Microbe, 2014, 15(6):768-778.
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