Resolvin E1 inhibits periodontitis and promotes reconstruction of periodontal tissue

doi:10.3969/j.issn.2095-4344.1114

Abstract

Abstract:

BACKGROUND: Resolvin E1 can effectively inhibit inflammatory cell infiltration and induce macrophages to
swallow 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.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Periodontitis, Inflammation, Pathology, Tissue Engineering

CLC Number:

R496

Cai Zhiguo, Liu Qi, Du Shasha, Yang Kun. Resolvin E1 inhibits periodontitis and promotes reconstruction of periodontal tissue[J]. Chinese Journal of Tissue Engineering Research, 2019, 23(11): 1794-1798.

Figures/Tables 1

References

[1] Molfino A, Amabile MI, Monti M, et al.Omega-3 Polyunsaturated Fatty Acids in Critical Illness: Anti-Inflammatory, Proresolving, or Both?. Oxid Med Cell Longev. 2017;2017:5987082.

[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 controlled- randomized 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 E2 and 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] Holmström SB, Clark R,Zwicker S,et al.Gingival Tissue Inflammation Promotes Increased Matrix Metalloproteinase-12 Production 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.