国际口腔医学杂志

国际口腔医学杂志 ›› 2018, Vol. 45 ›› Issue (4): 433-438.doi: 10.7518/gjkq.2018.04.011

• 综述 • 上一篇    下一篇

粪肠球菌与巨噬细胞相互作用机制的研究进展

林冬佳, 彭志翔, 高燕   

  1. 中山大学光华口腔医学院•附属口腔医院 广东省口腔医学重点实验室 广州 510055
  • 收稿日期:2017-12-06 修回日期:2018-04-17 出版日期:2018-07-02 发布日期:2018-07-02
  • 通讯作者: 高燕,副主任医师,硕士,Email：gaoyankq@aliyun.com
  • 作者简介:林冬佳,硕士,Email：doda.lin@foxmail.com
  • 基金资助:
    广东省自然科学基金（2016A030313267）

Progress in the interactive mechanism between Enterococcus faecalis and macrophages

Lin Dongjia, Peng Zhixiang, Gao Yan.   

  1. Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
  • Received:2017-12-06 Revised:2018-04-17 Online:2018-07-02 Published:2018-07-02
  • Supported by:
    This study was supported by Guangdong Provincial Natural Science Foundation (2016A030313267).

RichHTML

13

PDF (PC)

959

摘要： 粪肠球菌（Enterococcus faecalis）是难治性根尖周炎的主要致病菌,脂磷壁酸是其主要免疫原和重要毒力因子。作为天然免疫反应的重要成员,巨噬细胞在吞噬杀灭微生物、呈递抗原和分泌多种细胞因子调控机体的炎症反应等方面起了重要作用。粪肠球菌在与宿主巨噬细胞的长期相互作用过程中,也逐渐形成了多种逃避杀灭的有效策略,得以在宿主体内存活并增殖。本文就巨噬细胞抵抗粪肠球菌感染及粪肠球菌逃避巨噬细胞杀灭两方面的研究进展进行综述。

关键词: 粪肠球菌, 巨噬细胞, 根尖周炎

Abstract: Enterococcus faecalis is the main pathogen of refractory apical periodontitis. Lipoteichoic acid is the main immunogen and an important virulence factor of such infection. Macrophages, which are an important member of the natural immune response, are crucial in phagocytosis of microbes, presentation of antigens and secretion of various cytokines to regulate the inflammatory response of the body. In the long-term interaction with the host macrophages, E. faecalis gradually forms a variety of effective strategies for survival and proliferation. This review focuses on the resistance of macrophages to E. faecalis and the strategies of E. faecalis to avoid killing macrophages.

Key words: Enterococcus faecalis, macrophages, periodontitis

中图分类号: 

  • R780.2
[1] Gomes BP, Pinheiro ET, Jacinto RC, et al.Microbial analysis of canals of root-filled teeth with periapical lesions using polymerase chain reaction[J]. J Endod, 2008, 34(5): 537-540.
[2] Park OJ, Han JY, Baik JE, et al.Lipoteichoic acid of Enterococcus faecalis induces the expression of che-mokines via TLR2 and PAFR signaling pathways[J]. J Leukoc Biol, 2013, 94(6): 1275-1284.
[3] Graves DT, Oates T, Garlet GP.Review of osteoim-munology and the host response in endodontic and periodontal lesions[J]. J Oral Microbiol, 2011, 3(1): 5304.
[4] Zou J, Shankar N.The opportunistic pathogen Ente-rococcus faecalis resists phagosome acidification and autophagy to promote intracellular survival in macrophages[J]. Cell Microbiol, 2016, 18(6): 831-843.
[5] Locati M, Mantovani A, Sica A.Macrophage activa-tion and polarization as an adaptive component of innate immunity[J]. Adv Immunol, 2013, 120: 163-184.
[6] Park OJ, Han JY, Baik JE, et al.Lipoteichoic acid of Enterococcus faecalis induces the expression of che-mokines via TLR2 and PAFR signaling pathways[J]. J Leukoc Biol, 2013, 94(6): 1275-1284.
[7] Hong SW, Baik JE, Kang SS, et al.Lipoteichoic acid of Streptococcus mutans interacts with Toll-like re-ceptor 2 through the lipid moiety for induction of inflammatory mediators in murine macrophages[J]. Mol Immunol, 2014, 57(2): 284-291.
[8] Zou J, Shankar N.Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages[J]. Infect Immun, 2014, 82(12): 5132-5142.
[9] Coburn PS, Baghdayan AS, Dolan G, et al.An Ara C-type transcriptional regulator encoded on the Ente-rococcus faecalis pathogenicity island contributes to pathogenesis and intracellular macrophage survival[J]. Infect Immu, 2008, 76(12): 5668-5676.
[10] Mills CD.M1 and M2 macrophages: oracles of health and disease[J]. Crit Rev Immunol, 2012, 32(6): 463-488.
[11] Vogel DY, Glim JE, Stavenuiter AW, et al.Human macrophage polarization in vitro: maturation and activation methods compared[J]. Immunobiology, 2014, 219(9): 695-703.
[12] Yang J, Park OJ, Kim J, et al.Lipoteichoic acid of Enterococcus faecalis inhibits the differentiation of macrophages into osteoclasts[J]. J Endod, 2016, 42(4): 570-574.
[13] Prso IB, Kocjan W, Simić H, et al.Tumor necrosis factor-alpha and interleukin 6 in human periapical lesions[J]. Mediators Inflamm, 2007, 2007: 38210.
[14] Itoh T, Miyake Y, Onda A, et al.Immunomodulatory effects of heat-killed Enterococcus faecalis TH10 on murine macrophage cells[J]. Microbiologyopen, 2012, 1(4): 373-380.
[15] Lima SM, Sousa MG, Freire Mde S, et al.Immune response profile against persistent endodontic path-ogens Candida albicans and Enterococcus faecalis in vitro[J]. J Endod, 2015, 41(7): 1061-1065.
[16] Lee IT, Wang SW, Lee CW, et al.Lipoteichoic acid induces HO-1 expression via the TLR2/MyD88/c- Src/NADPH oxidase pathway and Nrf2 in human tracheal smooth muscle cells[J]. J Immunol, 2008, 181(7): 5098-5110.
[17] Baik JE, Ryu YH, Han JY, et al.Lipoteichoic acid partially contributes to the inflammatory responses to Enterococcus faecalis[J]. J Endod, 2008, 34(8): 975-982.
[18] Leendertse M, Willems RJ, Giebelen IA, et al.Peri-toneal macrophages are important for the early con-tainment of Enterococcus faecium peritonitis in mice[J]. Innate Immun, 2009, 15(1): 3-12.
[19] Yang Y, Wang X, Moore DR, et al.TNF-mediates macrophage-induced by stander effects through netrin-1[J]. Cancer Res, 2012, 72(20): 5219-5229.
[20] Benjamin JL, Sumpter R Jr, Levine B, et al.Intes-tinal epithelial autophagy is essential for host defense against invasive bacteria[J]. Cell Host Microbe, 2013, 13(6): 723-734.
[21] Cortes-Perez NG, Dumoulin R, Gaubert S, et al.Overexpression of Enterococcus faecalis elr operon protects from phagocytosis[J]. BMC Microbiol, 2015, 15: 112.
[22] Ellison DW, Miller VL.Regulation of virulence by members of the MarR/SlyA family[J]. Curr Opin Microbiol, 2006, 9(2): 153-159.
[23] Wu RY, Zhang RG, Zagnitko O, et al.Crystal structure of Enterococcus faecalis SlyA-like tran-scriptional factor[J]. J Biol Chem, 2003, 278(22): 20240-20244.
[24] Michaux C, Sanguinetti M, Reffuveille F, et al.SlyA is a transcriptional regulator involved in the virulence of Enterococcus faecalis[J]. Infect Immun, 2011, 79(7): 2638-2645.
[25] Forouhar F, Lee IS, Vujcic J, et al.Structural and functional evidence for Bacillus subtilis PaiA as a novel N1-spermidine/spermine acetyltransferase[J]. J Biol Chem, 2005, 280(48): 40328-40336.
[26] Martini C, Michaux C, Bugli F, et al.The polyamine N-acetyltransferase-like enzyme PmvE plays a role in the virulence of Enterococcus faecalis[J]. Infect Immun, 2015, 83(1): 364-371.
[27] Baik JE, Jang KS, Kang SS, et al.Calcium hydro-xide inactivates lipoteichoic acid from Enterococcus faecalis through deacylation of the lipid moiety[J]. J Endod, 2011, 37(2): 191-196.
[28] Hong SW, Baik JE, Kang SS, et al.Sodium hypo-chlorite inactivates lipoteichoic acid of Enterococcus faecalis by deacylation[J]. J Endod, 2016, 42(10): 1503-1508.
[29] Ashida H, Mimuro H, Ogawa M, et al.Cell death and infection: a double-edged sword for host and pathogen survival[J]. J Cell Biol, 2011, 195(6): 931-942.
[30] Gomes LC, Dikic I.Autophagy in antimicrobial immunity[J]. Mol Cell, 2014, 54(2): 224-233.
[31] Shoji-Kawata S, Sumpter R, Leveno M, et al.Identi-fication of a candidate therapeutic autophagy-indu-cing peptide[J]. Nature, 2013, 494(7436): 201-206.
[32] Campbell GR, Spector SA.Autophagy induction by vitamin D inhibits both Mycobacterium tuberculosis and human immunodeficiency virus type 1[J]. Auto-phagy, 2012, 8(10): 1523-1525.
[33] Choy A, Roy CR.Autophagy and bacterial infection: an evolving arms race[J]. Trends Microbiol, 2013, 21(9): 451-456.
[34] Detsch R, Boccaccini AR.The role of osteoclasts in bone tissue engineering[J]. J Tissue Eng Regen Med, 2015, 9(10): 1133-1149.
[35] Park OJ, Yang J, Kim J, et al.Enterococcus faecalis attenuates the differentiation of macrophages into osteoclasts[J]. J Endod, 2015, 41(5): 658-662.
[1] 徐智博,孟秀萍. 粪肠球菌逃逸宿主免疫防御机制的研究进展[J]. 国际口腔医学杂志, 2023, 50(5): 613-617.
[2] 梁芷瑩,赵苑汐,朱嘉妮,苏勤. 288例前牙显微根尖手术临床资料的回顾性分析[J]. 国际口腔医学杂志, 2023, 50(2): 166-171.
[3] 刘艺,刘奕. 巨噬细胞源性外泌体调控骨改建的研究进展[J]. 国际口腔医学杂志, 2023, 50(1): 120-126.
[4] 黄伟琨,徐秋艳,周婷. 黄芩苷抑制脂多糖促巨噬细胞氧化应激损伤作用的研究[J]. 国际口腔医学杂志, 2022, 49(5): 521-528.
[5] 朱嘉妮,苏勤. 难治性根尖周炎根管内及根尖外菌群的研究现状[J]. 国际口腔医学杂志, 2022, 49(3): 283-289.
[6] 刘千溪,吴佳益,任彪,黄睿洁. 粪肠球菌与口腔微生物相互作用的研究进展[J]. 国际口腔医学杂志, 2022, 49(3): 290-295.
[7] 赵玉洁,管晓燕,李小兰,陈琦君,王倩,刘建国. 巨噬细胞极化参与正畸牙移动的研究进展[J]. 国际口腔医学杂志, 2020, 47(4): 478-483.
[8] 刘晔,洪润丹,王志国,刘涵云,孟琛达,王茹,徐全臣. 人单核细胞和外周血单个核细胞衍生的巨噬细胞极化特性的比较[J]. 国际口腔医学杂志, 2020, 47(3): 286-292.
[9] 税钰森,吕潇颖,李静雅,杨燃. 粪肠球菌在口腔及全身系统性疾病中的致病相关因素及其机制的研究进展[J]. 国际口腔医学杂志, 2020, 47(2): 225-234.
[10] 崔钰嘉,孙建勋,周学东. 黄连素的生物学功能及治疗口腔疾病研究的进展[J]. 国际口腔医学杂志, 2020, 47(1): 115-120.
[11] 杨子,侯本祥. 持续性根尖周炎根管内外生物膜特性的研究进展[J]. 国际口腔医学杂志, 2019, 46(2): 238-243.
[12] 朱宸佑, 魏诗敏, 汪媛婧, 伍颖颖. 巨噬细胞在骨组织修复中的研究进展[J]. 国际口腔医学杂志, 2018, 45(4): 444-448.
[13] 吕晶, 凌均棨. 根管定位数字化导板的研究进展[J]. 国际口腔医学杂志, 2018, 45(2): 233-238.
[14] 衣晓伟, 黄定明, 张岚. 糖尿病患者牙髓根尖周病的发病机制及临床管理[J]. 国际口腔医学杂志, 2018, 45(2): 214-218.
[15] 黄月华, 唐晓琳. 单核-吞噬细胞系统与牙周炎关系的研究进展[J]. 国际口腔医学杂志, 2017, 44(5): 528-532.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] 张京剧. 青年期至中年期颅面复合体变化的头影测量研究[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 刘玲. 镍铬合金中铍对可铸造性和陶瓷金属结合力的影响[J]. 国际口腔医学杂志, 1999, 26(06): .
[3] 王昆润. 在种植体上制作固定义齿以后下颌骨密度的动态变化[J]. 国际口腔医学杂志, 1999, 26(06): .
[4] 王昆润. 重型颌面部炎症死亡和康复病例的实验室检查指标比较[J]. 国际口腔医学杂志, 1999, 26(06): .
[5] 逄键梁. 两例外胚层发育不良儿童骨内植入种植体后牙槽骨生长情况[J]. 国际口腔医学杂志, 1999, 26(05): .
[6] 温秀杰. 氟化物对牙本质脱矿抑制作用的体外实验研究[J]. 国际口腔医学杂志, 1999, 26(05): .
[7] 杨春惠. 耳颞神经在颞颌关节周围的分布[J]. 国际口腔医学杂志, 1999, 26(04): .
[8] 王昆润. 牙周炎加重期应选用何种抗生素[J]. 国际口腔医学杂志, 1999, 26(04): .
[9] 杨儒壮 孙宏晨 欧阳喈. 纳米级高分子支架材料在组织工程中的研究进展[J]. 国际口腔医学杂志, 2004, 31(02): 126 -128 .
[10] 严超然,李龙江. 肿瘤靶向药物载体系统的研究进展[J]. 国际口腔医学杂志, 2008, 35(S1): .