[1] XU R,ZENG G,WANG S,et al.Periodontitis promotes the diabetic development of obese rat via miR-147 induced classical macrophage activation[J].Biomed Pharmacother,2016,83:892-897. [2] 王琳源,关宁,林晓萍.Treg细胞介导的免疫应答在牙周炎小鼠中的研究[J].实用口腔医学杂志,2015,31(3):318-322. [3] 袁中政,刘引,申玉芹,等.牙周炎患者自身组织核酸对小鼠巨噬细胞中NLRP3 mRNA表达的影响及其意义[J].吉林大学学报(医学版),2019,45(1):23-27. [4] CEKICI A,KANTARCI A,HASTURK H,et al.Inflammatory and immune pathways in the pathogenesis of periodontal disease[J].Periodontology, 2014,64(1):57-80. [5] GORDON S, MARTINEZ F O. Alternative activation of macrophages:mechanism and functions[J]. Immunity, 2010, 32(5):593-604. [6] SIMA C, GLOGAUER M. Macrophage subsets and osteoimmunology:tuning of the immunological recognition and effector systems that maintain alveolar bone[J]. Periodontology, 2013, 63(1):80-101. [7] 梁红玲,陈斌,何莎莎,等.牙周炎和牙周健康状态的大鼠牙周组织中M1/M2型巨噬细胞的分布和比例[J].口腔疾病防治,2018,26(10):627-633. [8] 中华口腔医学会牙周病学专业委员会.重度牙周炎诊断标准及特殊人群牙周病治疗原则的中国专家共识[J].中华口腔医学杂志,2017,52(2):67-71. [9] STINGU C S,JENTSCH H,EICK S,et al. Microbial profile of patients with periodontitis compared with healthy subjects[J]. Quintessence Int, 2012,43(2):e23-e31. [10] 潘佳慧,唐秋玲,李格格,等.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[J].国际口腔医学杂志,2017,44(5):533-537. [11] JAGANNATHAN R, LAVU V, RAO S R. Comparison of the proportion of non-classic (CD14+CD16+) monocytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with chronic periodontitis[J].J Periodontol, 2014, 85(6):852-858. [12] OPPERMANN R V, WEIDLICH P, MUSSKOPF M L. Periodontal disease and systemic complications[J]. Braz Oral Res, 2012,26:39-47. [13] LAWRENCE T, NATOLI G. Transcriptional regulation of macrophage polarization:enabling diversity with identity[J]. Nat Rev Immunol, 2011, 11(11):750-761. [14] WHYTE C S, BISHOP E T, RUCKERL D, et al. Suppressor of cytokine signaling (SOCS)1 is a key determinant of differential macrophage activation and function[J]. J Leukoc Biol, 2011, 90(5):845-854. [15] MōGE J L, MEHRAJ V, CAPO C, et al. Macrophage polarization and bacterial infections[J]. Curr Opin Infect Dis, 2011, 24(3):230-234. [16] GEMMELL E, MCHUGH G B, GRIECO D A, et al. Costimulatory molecules in human periodontal disease tissues[J]. J Periodont Res, 2001, 36(2):92-100. [17] AALAEI-ANDABILI S H, 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. [18] HUSSAIN Q A, MCKAY I J, Gonzales-Marin C, et al. Detection of adrenomedullin and nitric oxide in different forms of periodontal disease[J]. J Periodont Res, 2016, 51(1):16-25. [19] ADLER H, FRECH B, THONY M, et al. Inducible nitric oxide synthase in cattle. Differential cytokine regulation of nitric oxide synthase in bovine and murine macrophages[J]. J Immunol, 1995,154(9):4710-4718. [20] HALL C J, BOYLE R H, ASTIN J W, et al. Immunoresponsive gene 1 augments bactericidal activity of macrophage-lineage cells by regulating β-oxidation-dependent mitochondrial ROS production[J]. Cell Metab, 2013, 18(2):265-278. [21] MURRAY PJ. The JAK -STAT signaling pathway:input and output integration[J]. J Immunol, 2007, 178(5):2623-2629. [22] HU J C, BROOKINGS W, ALDRIDGE M C. A case of solid pseudopapillary tumour of the pancreas and malignant mesothelioma[J]. J Gastrointest Cancer, 2007, 38(2/3/4):71-73. |