Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (5): 533-537.doi: 10.7518/gjkq.2017.05.008
• Periodontitis • Previous Articles Next Articles
Pan Jiahui, Tang Qiuling, Li Gege, Hou Yubo, Yu Weixian
CLC Number:
| [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. |