国际口腔医学杂志 ›› 2017, Vol. 44 ›› Issue (5): 533-537.doi: 10.7518/gjkq.2017.05.008

• 牙周专栏 • 上一篇    下一篇

巨噬细胞极化在牙龈卟啉单胞菌促进牙周炎发生发展中的作用

潘佳慧, 唐秋玲, 李格格, 侯玉帛, 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:2016-12-16 修回日期:2017-06-09 出版日期:2017-09-01 发布日期:2017-09-01
  • 通讯作者: 于维先,教授,博士,Email:yu-wei-xian@163.com
  • 作者简介:潘佳慧,硕士,Email:panjiahui0451@sina.com
  • 基金资助:

    吉林省科技厅自然科学基金项目(20150101076JC); 吉林省发展改革委员会科研项目(2013C022-4)

The role of macrophages polarization in the onset and development of periodontitis via Porphyromonas gingivalis

Pan Jiahui, Tang Qiuling, Li Gege, Hou Yubo, Yu Weixian   

  1. Dept. of Periodontology, Hospital of Stomatology, Jilin University;Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun 130021, China
  • Received:2016-12-16 Revised:2017-06-09 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) and Development and Reform Commission Scientific Foundation of Jilin Province(2013C022-4).

摘要:

牙龈卟啉单胞菌是牙周炎的主要致病菌,其侵袭牙周组织后引起大量炎症细胞浸润,并调控巨噬细胞极化,从而引发牙周组织的炎症反应。巨噬细胞具有很强的可塑性,在不同的微环境下可分化为具有不同表型和功能的细胞,此过程被称为巨噬细胞的极化。极化的巨噬细胞能够释放大量促炎因子,导致牙周组织的炎症反应,在牙周炎的发生、发展过程中起重要作用;同时又能产生某些杀菌物质,发挥其抗病原微生物的功能。本文就近年来巨噬细胞极化在牙周炎发生、发展过程中的作用进行综述。

关键词: 牙龈卟啉单胞菌, 巨噬细胞, 极化, 牙周炎

Abstract:

Porphyromonas gingivalis is the main pathogen causing periodontitis. Once invaded by Porphyromonas gingivalis, periodontal tissues become infiltrated by large amounts of inflammatory cells and undergo inflammation as macrophages polarize. Macrophages are characterized by considerable plasticity and can be divided into distinct functional cell phenotypes in different microenvironments. Polarized macrophages are essential for the onset and development of periodontitis. They can release a large number of inflammatory factors to damage periodontal tissues and produce some bactericidal substances to inhibit and kill pathogenic microbes. This review presents the role of macrophage polarization in the onset and development of periodontitis.

Key words: Prophyromonas gingivalis, macrophage, polarization, periodontitis

中图分类号: 

  • R781.4+2
[1] Murray PJ, Wynn TA. Protective and pathogenic functions of macrophage subsets[J]. Nat Rev Im-munol, 2011, 11(11):723-737.
[2] Jagannathan R, Lavu V, Rao SR. Comparison of the proportion of non-classic (CD14+CD16+) mono-cytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with chronic perio-dontitis[J]. J Periodontol, 2014, 85(6):852-858.
[3] Gemmell E, McHugh GB, Grieco DA, et al. Costimu-latory molecules in human periodontal disease tissues [J]. J Periodontal Res, 2001, 36(2):92-100.
[4] Gordon S, Martinez FO. Alternative activation of macrophages: mechanism and functions[J]. Immunity, 2010, 32(5):593-604.
[5] Lawrence T, Natoli G. Transcriptional regulation of macrophage polarization: enabling diversity with identity[J]. Nat Rev Immunol, 2011, 11(11):750-761.
[6] Mège JL, Mehraj V, Capo C. Macrophage polariza-tion and bacterial infections[J]. Curr Opin Infect Dis, 2011, 24(3):230-234.
[7] Hussain QA, McKay IJ, Gonzales-Marin C, et al. Detection of adrenomedullin and nitric oxide in dif-ferent forms of periodontal disease[J]. J Periodontal Res, 2016, 51(1):16-25.
[8] Mylonas KJ, Jenkins SJ, Castellan RF, et al. The adult murine heart has a sparse, phagocytically active macrophage population that expands through mono-cyte recruitment and adopts an ‘M2’ phenotype in response to Th2 immunologic challenge[J]. Immuno-biology, 2015, 220(7):924-933.
[9] Spiller KL, Nassiri S, Witherel CE, et al. Sequential delivery of immunomodulatory cytokines to facilitate the M1-to-M2 transition of macrophages and enhance vascularization of bone scaffolds[J]. Biomaterials, 2015, 37:194-207.
[10] Lam RS, O'Brien-Simpson NM, Lenzo JC, et al. Ma-crophage depletion abates Porphyromonas gingivalis - induced alveolar bone resorption in mice[J]. J Immunol, 2014, 193(5):2349-2362.
[11] Hajishengallis G, Darveau RP, Curtis MA. The keys-tone-pathogen hypothesis[J]. Nat Rev Microbiol, 2012, 10(10):717-725.
[12] Holden JA, Attard TJ, Laughton KM, et al. Porphyro - monas gingivalis lipopolysaccharide weakly activates M1 and M2 polarized mouse macrophages but in-duces inflammatory cytokines[J]. Infect Immun, 2014, 82(10):4190-4203.
[13] Mysak J, Podzimek S, Sommerova P, et al. Porphyro - monas gingivalis : major periodontopathic pathogen overview[J]. J Immunol Res, 2014, 163(3):234-243.
[14] Jain S, Coats SR, Chang AM, et al. A novel class of lipoprotein lipase-sensitive molecules mediates Toll-like receptor 2 activation by Porphyromonas gin-givalis [J]. Infect Immun, 2013, 81(4):1277-1286.
[15] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44.
[16] Aalaei-andabili SH, Rezaei N. Toll like receptor (TLR)-induced differential expression of microRNAs (MiRs) promotes proper immune response against infections: a systematic review[J]. J Infect, 2013, 67(4):251-264.
[17] Essandoh K, Fan GC. Role of extracellular and intra-cellular microRNAs in sepsis[J]. Biochim Biophys Acta, 2014, 1842(11):2155-2162.
[18] Tipton DA, Cho S, Zacharia N, et al. Inhibition of interleukin-17-stimulated interleukin-6 and -8 pro-duction by cranberry components in human gingival fibroblasts and epithelial cells[J]. J Periodontal Res, 2013, 48(5):638-646.
[19] Yamauchi K, Shibata Y, Kimura T, et al. Azithro-mycin suppresses interleukin-12p40 expression in lipopolysaccharide and interferon-γ stimulated macro-phages[J]. Int J Biol Sci, 2009, 5(7):667-678.
[20] Tipton DA, Babu JP, Dabbous MKh. Effects of cran-berry components on human aggressive periodontitis gingival fibroblasts[J]. J Periodontal Res, 2013, 48 (4):433-442.
[21] Bostanci N, Belibasakis GN. Porphyromonas gin-givalis : an invasive and evasive opportunistic oral pathogen[J]. FEMS Microbiol Lett, 2012, 333(1):1-9.
[22] Hajishengallis G. Immuno-microbial pathogenesis of periodontitis: keystones, pathobionts, and host re-sponse[J]. Trends Immunol, 2014, 35(1):3-11.
[23] Wang M, Krauss JL, Domon H, et al. Microbial hijacking of complement-Toll-like receptor crosstalk [J]. Sci Signal, 2010, 3(109):ra11.
[24] Hajishengallis G. Complement and periodontitis[J]. Biochem Pharmacol, 2010, 80(12):1992-2001.
[25] Kolev M, Le Friec G, Kemper C. Complement—tapping into new sites and effector systems[J]. Nat Rev Immunol, 2014, 14(12):811-820.
[26] Morgan TM, Koreckij TD, Corey E. Targeted therapy for advanced prostate cancer: inhibition of the PI3K/Akt/mTOR pathway[J]. Curr Cancer Drug Targets, 2009, 9(2):237-249.
[27] Quan JH, Chu JQ, Kwon J, et al. Intracellular networks of the PI3K/AKT and MAPK pathways for regulating Toxoplasma gondii -induced IL-23 and IL-12 pro-duction in human THP-1 cells[J]. PLoS One, 2015, 10(11):e0141550.
[28] Hickey FB, Brereton CF, Mills KH. Adenylate cycalse toxin of Bordetella pertussis inhibits TLR-induced IRF-1 and IRF-8 activation and IL-12 production and enhances IL-10 through MAPK activation in dendritic cells[J]. J Leukoc Biol, 2008, 84(1):234-243.
[29] Liang S,Krauss JL,Domon H, et al. The C5a rece-ptor impairs IL-12-dependent clearance of Porphy - romonas gingivalis and is required for induction of periodontal bone loss[J]. J Immunol, 2011, 186(2): 869-877.
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