消退素E1抑制牙周炎及促进牙周组织重建的作用
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摘要
背景:E-系列消退素1(Resolvin E1,RvE1)能有效抑制炎性细胞浸润、诱导巨噬细胞吞噬体内有害物质等,促进炎症消退的作用,在实验性牙周炎病理转归中的效果已经得到初步证实。目的:综述了消退素E1对牙周炎病理转归的促进作用及潜在的意义。方法:以"消退素E1,牙周炎,白细胞,血小板,活性氧,巨噬细胞,炎性因子,成骨细胞,破骨细胞"和"Resolvin E1, Periodontitis,leukocyte,platelet,reactive oxygen species,Macrophages,inflammatory factor,osteoblast,osteoclast"为关键词,检索PubMed数据库、中国生物医学文献库(CBM)和中国知识资源总库(CNKI)系列数据库1996年至2018年间收录的消退素E1与牙周炎相关文献33条,分析消退素E1对牙周炎修复和再生的研究进展。结果与结论:目前临床途径尚不能有效解决牙周组织炎性反应、不可逆性丧失等难题,迫切需要有效途径控制炎症反应、恢复牙周重建。近年来大量研究显示消退素E1在牙周炎动物及细胞模型病理转归中具有良好的效果。消退素E1作为特定G蛋白偶联受体(趋化素受体23,白三烯B4受体1)的激动剂或部分激动剂,可以引发一系列细胞特异性反应,反向调节炎症进展,将可能为牙周炎病理转归提供新的方向。
BACKGROUND: Resolvin E1 can effectively inhibit inflammatory cell infiltration and induce macrophages toswallow hazardous substances, and thus alleviates inflammation. Moreover, its effect on improving periodontitis has been preliminarily confirmed. OBJECTIVE: To review the effects of resolvin E1 on promoting the pathologic regression of periodontitis and its potential significance. METHODS: Articles addressing resolvin E1 and periodontitis published from 1996 to 2018 were retrieved from PubMed, CBM and CNKI databases. The keywords were "resolving E1, periodontitis, leukocyte, platelet, reactive oxygen species, macrophages, inflammatory factor, osteoblast, osteoclast" in English and Chinese, respectively. Thirty-three articles were included to analyze the research advance regarding resolvin E1 in the repair of periodontitis and tissue regeneration. RESULTS AND CONCLUSION: At present, the clinical therapeutic pathway cannot solve the inflammatory reaction and irreversible loss of periodontal tissue effectively, so an effective way to control the inflammatory process and treat periodontitis is urgently needed. In recent years, a large number of studies have shown that resolvin E1 has a good therapeutic effect on periodontitis in animals and cell models. Resolvin E1, as an agonist or partial agonist of specific G protein-coupled receptor(chemokine receptor 23, leukotriene B4), can trigger a series of specific responses and reverse inflammation progression, which may provide a new direction for inversing the pathology of periodontal disease.
BACKGROUND: Resolvin E1 can effectively inhibit inflammatory cell infiltration and induce macrophages toswallow hazardous substances, and thus alleviates inflammation. Moreover, its effect on improving periodontitis has been preliminarily confirmed. OBJECTIVE: To review the effects of resolvin E1 on promoting the pathologic regression of periodontitis and its potential significance. METHODS: Articles addressing resolvin E1 and periodontitis published from 1996 to 2018 were retrieved from PubMed, CBM and CNKI databases. The keywords were "resolving E1, periodontitis, leukocyte, platelet, reactive oxygen species, macrophages, inflammatory factor, osteoblast, osteoclast" in English and Chinese, respectively. Thirty-three articles were included to analyze the research advance regarding resolvin E1 in the repair of periodontitis and tissue regeneration. RESULTS AND CONCLUSION: At present, the clinical therapeutic pathway cannot solve the inflammatory reaction and irreversible loss of periodontal tissue effectively, so an effective way to control the inflammatory process and treat periodontitis is urgently needed. In recent years, a large number of studies have shown that resolvin E1 has a good therapeutic effect on periodontitis in animals and cell models. Resolvin E1, as an agonist or partial agonist of specific G protein-coupled receptor(chemokine receptor 23, leukotriene B4), can trigger a series of specific responses and reverse inflammation progression, which may provide a new direction for inversing the pathology of periodontal disease.
引文
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[9]Da YO,Talukdar S,Bae EJ,et al.GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects.Cell.2010;142(5):687-698.
[10]Dai J,Bi L, Lin J, et al. Evaluation of interleukin-10 producing CD19+B cells in human gingival tissue. Arch Oral Biol. 2017;84:112-117.
[11]Roberts HM,Ling MR,Insall R,et al.Impaired neutrophil directional chemotactic accuracy in chronic periodontitis patients.J Clin Periodontol. 2015;42(1):1-11.
[12]Arita M,Yoshida M,Hong S,et al.Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Proc Natl Acad Sci U S A.2005;102(21):7671-7676.
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[14]Fredman G, Oh SF, Ayilavarapu S, et al.Impaired phagocytosis in localized aggressive periodontitis:rescue by Resolvin E1.PLoS One. 2011;6(9):e24422.
[15]Dona M,Fredman G,Schwab JM, et al.Resolvin E1, an EPA-derived mediator in whole blood, selectively counterregulates leukocytes and platelets.Blood.2008;112(3):848.
[16]Lee CT,Teles R, Kantarci A,et al.Resolvin E1 Reverses Experimental Periodontitis and Dysbiosis. J Immunol. 2016;197(7):2796-2806.
[17]Fredman G,Dyke T E V, Serhan CN. Resolvin E1 regulates adenosine diphosphate activation of human platelets.Arterioscler Thromb Vasc Biol. 2010;30(10):2005-2013.
[18]Arvanitidis E,Bizzarro S,Rodriguez EA,et al.Reduced platelet hyper-reactivity and platelet-leukocyte aggregation after periodontal therapy. Thromb J. 2017;15:5.
[19]Laky M,Anscheringer I,Wolschner L,et al.Periodontal treatment limits platelet activation in patients with periodontitis-a controlledrandomized intervention trial. J Clin Periodontol. 2018;45(9):1090-1097.
[20]Henry MN, Peter S, Harald FL. Platelets in inflammation and at herogenesis.FrontImmunol.2015; 6(98):1-11.
[21]Hajishengallis G,Moutsopoulos NM,Hajishengallis E,et al. Immune and regulatory functions of neutrophils in inflammatory bone loss.Semin Immunol. 2016;28(2):146-158.
[22]Unno Y, Sato Y, Fukuda H, et al. Resolvin E1, but not resolvins E2and E3, promotes fMLF-induced ROS generation in human neutrophils. FEBS Lett. 2018;592(16):2706-2715.
[23]Hasturk H,Kantarci A,Ohira T,et al. Resolvin E1 protects from local inflammation and osteoclast-mediated bone destruction in periodontitis. FASEB J.2006;20(2):401-403.
[24]Ortega-Gómez A, Perretti M, Soehnlein O. Resolution of inflammation:an integrated view. EMBO Mol Med.2013;5(5):661-674.
[25]Holmstr?m SB, Clark R,Zwicker S,et al.Gingival Tissue Inflammation Promotes Increased Matrix Metalloproteinase-12Production by CD200R(low)Monocyte-Derived Cells in Periodontitis.J Immunol. 2017;199(12):4023-4035..
[26]Italiani P,Boraschi D.From monocytes to M1/M2 macrophages:phenotypical vs. Front Immunol. 2014;5:514.
[27]Van den Bossche J, Baardman J, Otto NA, et al.Mitochondrial dysfunction prevents repolarization of inflammatory macrophages.Cell Rep.2016;17(3):684–696.
[28]Moutsopoulos N, Konkel J, Sarmadi M, et al. Defective neutrophil recruitment in leukocyte adhesion deficiency type I disease causes local IL-17-driven inflammatory bone loss.Sci Transl Med.2014;6(229):229ra40..
[29]Davies LC,Taylor PR.Tissue-resident macrophages:then and now.Immunology.2015;144(4):541-548.
[30]Gao L,Faibish D,Fredman G,et al.Resolvin E1 and chemokine-like receptor 1 mediate bone preservation. J Immunol. 2013;190(2):689-694.
[31]Crotti TN,Dharmapatni AA,Alias E,et al.Osteoimmunology:Major and Costimulatory Pathway Expression Associated with Chronic Inflammatory Induced Bone Loss. J Immunol Res. 2015;2015:281287.
[32]Bostanci N, Saygan B, Emingil G,et al.Effect of periodontal treatment on receptor activator of NF-κB ligand and osteoprotegerin levels and relative ratio in gingival crevicular fluid.J Clin Periodontol. 2011;38(5):428-433.
[33]Cerletti C,de Gaetano G,Lorenzet R.Platelet–leukocyte interactions:multiple links between inflammation, blood coagulation and vascular risk.Mediterr J Hematol Infect Dis.2010;2(3):e2010023.
[2]Uddin M, Levy BD.Resolvins:natural agonists for resolution of pulmonary inflammation.Prog Lipid Res.2011;50(1):75-88.
[3]Balta MG, Loos BG, Nicu EA. Emerging Concepts in the Resolution of Periodontal Inflammation:A Role for Resolvin E1.Front Immunol. 2017;8:1682.
[4]Spite M,Serhan CN. Novel lipid mediators promote resolution of acute inflammation:impact of aspirin and statins. Circ Res. 2010;107(10):1170-1184.
[5]Haas-Stapleton EJ,Yan L,Song H,et al.Candida albicansModulates Host Defense by Biosynthesizing the Pro-Resolving Mediator Resolvin E1.Plos One.2007;2(12):e1316.
[6]Arita M,Bianchini F,Aliberti J,et al.Stereochemical assignment,antiinflammatory properties, and receptor for the omega-3 lipid mediator resolvin E1.J exp med.2005;201(5):713-722.
[7]Alessi DR,Caudwell FB,Andjelkovic M,et al. Molecular basis for the substrate specificity of protein kinase B; comparison with MAPKAP kinase-1 and p70 S6 kinase. FEBS Lett.1996;399(3):333-338.
[8]Loos BG,Papantonopoulos G,Jepsen S,et al.What is the Contribution of Genetics to Periodontal Risk?. Dent Clin North Am.2015;59(4):761-780.
[9]Da YO,Talukdar S,Bae EJ,et al.GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects.Cell.2010;142(5):687-698.
[10]Dai J,Bi L, Lin J, et al. Evaluation of interleukin-10 producing CD19+B cells in human gingival tissue. Arch Oral Biol. 2017;84:112-117.
[11]Roberts HM,Ling MR,Insall R,et al.Impaired neutrophil directional chemotactic accuracy in chronic periodontitis patients.J Clin Periodontol. 2015;42(1):1-11.
[12]Arita M,Yoshida M,Hong S,et al.Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Proc Natl Acad Sci U S A.2005;102(21):7671-7676.
[13]Hajishengallis E, Hajishengallis G.Neutroph IL. Neutrophil homeostasis and periodontal health in children and adults. J Dent Res. 2014;93(3):231-237.
[14]Fredman G, Oh SF, Ayilavarapu S, et al.Impaired phagocytosis in localized aggressive periodontitis:rescue by Resolvin E1.PLoS One. 2011;6(9):e24422.
[15]Dona M,Fredman G,Schwab JM, et al.Resolvin E1, an EPA-derived mediator in whole blood, selectively counterregulates leukocytes and platelets.Blood.2008;112(3):848.
[16]Lee CT,Teles R, Kantarci A,et al.Resolvin E1 Reverses Experimental Periodontitis and Dysbiosis. J Immunol. 2016;197(7):2796-2806.
[17]Fredman G,Dyke T E V, Serhan CN. Resolvin E1 regulates adenosine diphosphate activation of human platelets.Arterioscler Thromb Vasc Biol. 2010;30(10):2005-2013.
[18]Arvanitidis E,Bizzarro S,Rodriguez EA,et al.Reduced platelet hyper-reactivity and platelet-leukocyte aggregation after periodontal therapy. Thromb J. 2017;15:5.
[19]Laky M,Anscheringer I,Wolschner L,et al.Periodontal treatment limits platelet activation in patients with periodontitis-a controlledrandomized intervention trial. J Clin Periodontol. 2018;45(9):1090-1097.
[20]Henry MN, Peter S, Harald FL. Platelets in inflammation and at herogenesis.FrontImmunol.2015; 6(98):1-11.
[21]Hajishengallis G,Moutsopoulos NM,Hajishengallis E,et al. Immune and regulatory functions of neutrophils in inflammatory bone loss.Semin Immunol. 2016;28(2):146-158.
[22]Unno Y, Sato Y, Fukuda H, et al. Resolvin E1, but not resolvins E2and E3, promotes fMLF-induced ROS generation in human neutrophils. FEBS Lett. 2018;592(16):2706-2715.
[23]Hasturk H,Kantarci A,Ohira T,et al. Resolvin E1 protects from local inflammation and osteoclast-mediated bone destruction in periodontitis. FASEB J.2006;20(2):401-403.
[24]Ortega-Gómez A, Perretti M, Soehnlein O. Resolution of inflammation:an integrated view. EMBO Mol Med.2013;5(5):661-674.
[25]Holmstr?m SB, Clark R,Zwicker S,et al.Gingival Tissue Inflammation Promotes Increased Matrix Metalloproteinase-12Production by CD200R(low)Monocyte-Derived Cells in Periodontitis.J Immunol. 2017;199(12):4023-4035..
[26]Italiani P,Boraschi D.From monocytes to M1/M2 macrophages:phenotypical vs. Front Immunol. 2014;5:514.
[27]Van den Bossche J, Baardman J, Otto NA, et al.Mitochondrial dysfunction prevents repolarization of inflammatory macrophages.Cell Rep.2016;17(3):684–696.
[28]Moutsopoulos N, Konkel J, Sarmadi M, et al. Defective neutrophil recruitment in leukocyte adhesion deficiency type I disease causes local IL-17-driven inflammatory bone loss.Sci Transl Med.2014;6(229):229ra40..
[29]Davies LC,Taylor PR.Tissue-resident macrophages:then and now.Immunology.2015;144(4):541-548.
[30]Gao L,Faibish D,Fredman G,et al.Resolvin E1 and chemokine-like receptor 1 mediate bone preservation. J Immunol. 2013;190(2):689-694.
[31]Crotti TN,Dharmapatni AA,Alias E,et al.Osteoimmunology:Major and Costimulatory Pathway Expression Associated with Chronic Inflammatory Induced Bone Loss. J Immunol Res. 2015;2015:281287.
[32]Bostanci N, Saygan B, Emingil G,et al.Effect of periodontal treatment on receptor activator of NF-κB ligand and osteoprotegerin levels and relative ratio in gingival crevicular fluid.J Clin Periodontol. 2011;38(5):428-433.
[33]Cerletti C,de Gaetano G,Lorenzet R.Platelet–leukocyte interactions:multiple links between inflammation, blood coagulation and vascular risk.Mediterr J Hematol Infect Dis.2010;2(3):e2010023.