Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (5): 519-522.doi: 10.7518/gjkq.2017.05.005

• Periodontitis • Previous Articles     Next Articles

Immune evasion strategies of Porphyromonas gingivalis via gingipains

Li Gege1, Pan Jiahui1, Tang Qiuling1, Liu Xinchan2, Hou Yubo1, Yu Weixian1   

  1. 1. Dept. of Periodontology, Hospital of Stomatology, Jilin University; Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun 130021, China;
    2. Dept. of Dental Implantology, Hospital of Stomatology, Jilin University;Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun 130021, China
  • Received:2016-11-19 Revised:2017-05-16 Online:2017-09-01 Published:2017-09-01
  • Supported by:

    ; This study was supported by Funding from the Jilin Provincial Science and Technology Department(20150101076JC), Jilin Provincial Technology Innovation Projects(2016J073) and National Natural Science Foundation of China(81570983).

Abstract:

The keystone-pathogen hypothesis about the etiology of periodontitis has attracted the attention of scholars in recent years. In this view, Porphyromonas gingivalis is considered as a keystone pathogen in the pathogenic progression of periodontitis. Gingipains generated by Porphyromonas gingivalis are key virulence factors, which could assist Porphyromonas gingivalis to escape the killing effects of macrophages, neutrophils and complement system. The aim of this literature review is to discuss the immune evasion strategies ofPorphyromonas gingivalis via gingipains. The exposition of this important mechanism may provide a further understanding of the pathogenic mechanism of gingipains, and lay a foundation for exploring new methods for the prevention and treatment of periodontitis.

Key words: periodontitis, Prophyromonas gingivalis, gingipain, immune evasion

CLC Number: 

  • R780.2

TrendMD: 
[1] Hajishengallis G, Darveau RP, Curtis MA. The keys-tone-pathogen hypothesis[J]. Nat Rev Microbiol, 2012, 10(10):717-725.
[2] Hajishengallis G, Lamont RJ. Dancing with the stars: how choreographed bacterial interactions dictate nososymbiocity and give rise to keystone pathogens, accessory pathogens, and pathobionts[J]. Trends Microbiol, 2016, 24(6):477-489.
[3] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44.
[4] Benedyk M, Mydel PM, Delaleu N, et al. Gingipains: critical factors in the development of aspiration pneumonia caused by Porphyromonas gingivalis [J]. J Innate Immun, 2016, 8(2):185-198.
[5] Potempa J, Pike R, Travis J. Titration and mapping of the active site of cysteine proteinases from Por-phyromonas gingivalis (gingipains) using peptidyl chloromethanes[J]. Biol Chem, 1997, 378(3/4):223- 230.
[6] Potempa J, Pike R, Travis J. The multiple forms of trypsin-like activity present in various strains of Por-phyromonas gingivalis are due to the presence of either Arg-gingipain or Lys-gingipain[J]. Infect Im-mun, 1995, 63(4):1176-1182.
[7] Wang M, Krauss JL, Domon H, et al. Microbial hijacking of complement-toll-like receptor crosstalk [J]. Sci Signal, 2010, 3(109):ra11.
[8] Hajishengallis G, Abe T, Maekawa T, et al. Role of complement in host-microbe homeostasis of the pe-riodontium[J]. Semin Immunol, 2013, 25(1):65-72.
[9] Hussain QA, McKay IJ, Gonzales-Marin C, et al. Detection of adrenomedullin and nitric oxide in dif-ferent forms of periodontal disease[J]. J Periodont Res, 2016, 51(1):16-25.
[10] Liang S, Krauss JL, Domon H, et al. The C5a rece-ptor impairs IL-12-dependent clearance of Porphyro-monas gingivalis and is required for induction of periodontal bone loss[J]. J Immunol, 2011, 186(2): 869-877.
[11] Hawlisch H, Belkaid Y, Baelder R, et al. C5a nega-tively regulates toll-like receptor 4-induced immune responses[J]. Immunity, 2005, 22(4):415-426.
[12] Wu Z, Liu Y, Dong W, et al. CD14 in the TLRs signaling pathway is associated with the resistance to E. coli F18 in Chinese domestic weaned piglets[J]. Sci Rep, 2016, 6:24611.
[13] Holden JA, Attard TJ, Laughton KM, et al. Por-phyromonas gingivalis lipopolysaccharide weakly activates M1 and M2 polarized mouse macrophages but induces inflammatory cytokines[J]. Infect Immun, 2014, 82(10):4190-4203.
[14] Lam RS, O’Brien-Simpson NM, Holden JA, et al. Unprimed, M1 and M2 macrophages differentially interact with Porphyromonas gingivalis [J]. PLoS ONE, 2016, 11(7):e0158629.
[15] Wilensky A, Tzach-Nahman R, Potempa J, et al. Porphyromonas gingivalis gingipains selectively reduce CD14 expression, leading to macrophage hyporesponsiveness to bacterial infection[J]. J Innate Immun, 2015, 7(2):127-135.
[16] Abe T, Hosur KB, Hajishengallis E, et al. Local com-plement-targeted intervention in periodontitis: proof-of-concept using a C5a receptor(CD88) antagonist [J]. J Immunol, 2012, 189(11):5442-5448.
[17] Kataoka S, Baba A, Suda Y, et al. A novel, potent dual inhibitor of Arg-gingipains and Lys-gingipain as a promising agent for periodontal disease therapy [J]. FASEB J, 2014, 28(8):3564-3578.
[18] Reynolds EC, O’Brien-Simpson N, Rowe T, et al. Prospects for treatment of Porphyromonas gingiva-lis -mediated disease—immune-based therapy[J]. J Oral Microbiol, 2015, 7:29125.
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