Int J Stomatol

Int J Stomatol ›› 2023, Vol. 50 ›› Issue (5): 613-617.doi: 10.7518/gjkq.2023073

• Reviews • Previous Articles     Next Articles

Research progress on mechanism of Enterococcus faecalis escaping host immune defense

Xu Zhibo(),Meng Xiuping.()   

  1. Dept. of Cariology and Endodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China
  • Received:2022-10-15 Revised:2023-03-06 Online:2023-09-01 Published:2023-09-01
  • Contact: Xiuping. Meng E-mail:xuzb21@mails.jlu.edu.cn;mengxp@jlu.edu.cn

RichHTML

14

PDF (PC)

518

Abstract:

Enterococcus faecalis is the main pathogenic bacteria in persistent apical periodontitis, which contains a variety of virulence factors. The host immune defense can mobilize a variety of immune cells and immune molecules in the body to regulate the body’s inflammatory response, which can play an important role in persistent periapical periodontitis caused by Enterococcus faecalisis. However, in the process of invading the body, Enterococcus faecalisis can form a va-riety of mechanisms to escape host defense immunity, so that it can survive in the host and cause damage. This article will review the research progress on the immune defense mechanism of Enterococcus faecalisis escaping the host, aiming to explore why Enterococcus faecalisis cannot be cleared in the periapical tissue from the perspective of immunity, in order to provide new information for the prevention and treatment of persistent periapical periodontitis idea.

Key words: Enterococcus faecalis, immune evasion, periodontitis

CLC Number: 

  • Q 939.93

TrendMD: 
1 Siqueira JF Jr, Antunes HS, Pérez AR, et al. The apical root canal system of teeth with posttreatment apical periodontitis: correlating microbiologic, tomographic, and histopathologic findings[J]. J Endod, 2020, 46(9): 1195-1203.
2 Çalışkan MK, Kaval ME, Tekin U, et al. Radiographic and histological evaluation of persistent periapical lesions associated with endodontic fai-lures after apical microsurgery[J]. Int Endod J, 2016, 49(11): 1011-1019.
3 Yin M, Zhang Y, Li H. Advances in research on immunoregulation of macrophages by plant polysaccharides[J]. Front Immunol, 2019, 10: 145.
4 Urusova DV, Merriman JA, Gupta A, et al. Rifampin resistance mutations in the rpoB gene of Enterococcus faecalis impact host macrophage cytokine production[J]. Cytokine, 2022, 151: 155788.
5 Wang S, Liu K, Seneviratne CJ, et al. Lipoteichoic acid from an Enterococcus faecalis clinical strain pro-motes TNF-α expression through the NF-κB and p38 MAPK signaling pathways in differentiated THP-1 macrophages[J]. Biomed Rep, 2015, 3(5): 697-702.
6 Zou J, Shankar N. The opportunistic pathogen Enterococcus faecalis resists phagosome acidification and autophagy to promote intracellular survival in ma-crophages[J]. Cell Microbiol, 2016, 18(6): 831-843.
7 Lin PW, Chu ML, Liu HS. Autophagy and metabolism[J]. Kaohsiung J Med Sci, 2021, 37(1): 12-19.
8 Daw K, Baghdayan AS, Awasthi S, et al. Biofilm and planktonic Enterococcus faecalis elicit different responses from host phagocytes in vitro [J]. FEMS Immunol Med Microbiol, 2012, 65(2): 270-282.
9 Baldassarri L, Bertuccini L, Creti R, et al. Glycosaminoglycans mediate invasion and survival of Enterococcus faecalis into macrophages[J]. J Infect Dis, 2005, 191(8): 1253-1262.
10 Lacey DL, Timms E, Tan HL, et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation[J]. Cell, 1998, 93(2): 165-176.
11 Xu ZZ, Tong ZC, Neelakantan P, et al. Enterococcus faecalis immunoregulates osteoclastogenesis of macrophages[J]. Exp Cell Res, 2018, 362(1): 152-158.
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 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.
14 孙鹏, 陈敏, 张细六, 等. 虎杖苷通过调控HMGB1/TLR4/NF-κB信号通路对脓毒症急性肺损伤的保护作用[J]. 浙江中医药大学学报, 2021, 45(7): 691-699.
Sun P, Chen M, Zhang XL, et al. The protective effect of polydatin on sepsis-induced acute lung injury in rats by regulating HMGB1/TLR4/NF-κB signa-ling pathway[J]. J Zhejiang Chin Med Univ, 2021, 45(7): 691-699.
15 唐秋玲, 李格格, 潘佳慧, 等. 细胞焦亡与牙龈卟啉单胞菌的关系及其在牙周病发生发展中的作用机制[J]. 国际口腔医学杂志, 2017, 44(6): 660-663.
Tang QL, Li GG, Pan JH, et al. Mechanism of pyroptosis and Porphyromonas gingivalis in periodontitis development process[J]. Int J Stomatol, 2017, 44(6): 660-663.
16 D’Arcy MS. Cell death: a review of the major forms of apoptosis, necrosis and autophagy[J]. Cell Biol Int, 2019, 43(6): 582-592.
17 He DW, Li XY, Zhang FZ, et al. Dec2 inhibits ma-crophage pyroptosis to promote periodontal homeostasis[J]. J Periodontal Implant Sci, 2022, 52(1): 28-38.
18 Wang LN, Jin HW, Ye DD, et al. Enterococcus faecalis lipoteichoic acid-induced NLRP3 inflammasome via the activation of the nuclear factor kappa B pathway[J]. J Endod, 2016, 42(7): 1093-1100.
19 Ran SJ, Huang J, Liu B, et al. Enterococcus Faecalis activates NLRP3 inflammasomes leading to increased interleukin-1 beta secretion and pyroptosis of THP-1 macrophages[J]. Microb Pathog, 2021, 154: 104761.
20 Evavold CL, Ruan JB, Tan YH, et al. The pore-forming protein gasdermin D regulates interleukin-1 secretion from living macrophages[J]. Immunity, 2018, 48(1): 35.e6-44.e6.
21 Burn GL, Foti A, Marsman G, et al. The neutrophil[J]. Immunity, 2021, 54(7): 1377-1391.
22 Vanek NN, Simon SI, Jacques-Palaz K, et al. Enterococcus faecalis aggregation substance promotes opsonin-independent binding to human neutrophils via a complement receptor type 3-mediated mechanism[J]. FEMS Immunol Med Microbiol, 1999, 26(1): 49-60.
23 Rakita RM, Vanek NN, Jacques-Palaz K, et al. Enterococcus faecalis bearing aggregation substance is resistant to killing by human neutrophils despite phagocytosis and neutrophil activation[J]. Infect Immun, 1999, 67(11): 6067-6075.
24 Smith RE, Salamaga B, Szkuta P, et al. Decoration of the enterococcal polysaccharide antigen EPA is essential for virulence, cell surface charge and interaction with effectors of the innate immune system[J]. PLoS Pathog, 2019, 15(5): e1007730.
25 Shon W, Lim S, Bae KS, et al. The expression of alpha4 integrins by human polymorphonuclear neutrophils in response to sonicated extracts of Enterococcus faecalis [J]. J Endod, 2005, 31(5): 369-372.
26 Qian C, Cao XT. Dendritic cells in the regulation of immunity and inflammation[J]. Semin Immunol, 2018, 35: 3-11.
27 Elashiry MM, Elashiry M, Zeitoun R, et al. Enterococcus faecalis induces differentiation of immune-aberrant dendritic cells from murine bone marrow-derived stem cells[J]. Infect Immun, 2020, 88(11): e00338-e00320.
28 Kathirvel S, Mani M, Gopala Krishnan GK, et al. Molecular characterization of Enterococcus faecalis isolates from urinary tract infection and interaction between Enterococcus faecalis encountered dendri-tic and natural killer cells[J]. Microb Pathog, 2020, 140: 103944.
29 Furrie E, MacFarlane S, Cummings JH, et al. Systemic antibodies towards mucosal bacteria in ulce-rative colitis and Crohn’s disease differentially activate the innate immune response[J]. Gut, 2004, 53(1): 91-98.
30 Park SY, Shin YP, Kim CH, et al. Immune evasion of Enterococcus faecalis by an extracellular gelati-nase that cleaves C3 and iC3b[J]. J Immunol, 2008, 181(9): 6328-6336.
31 Ali YM, Sim RB, Schwaeble W, et al. Enterococcus faecalis escapes complement-mediated killing via recruitment of complement factor H[J]. J Infect Dis, 2019, 220(6): 1061-1070.
32 Harvey BS, Baker CJ, Edwards MS. Contributions of complement and immunoglobulin to neutrophil-mediated killing of enterococci[J]. Infect Immun, 1992, 60(9): 3635-3640.
33 Benachour A, Ladjouzi R, Le Jeune A, et al. The lysozyme-induced peptidoglycan N-acetylglucosamine deacetylase PgdA (EF1843) is required for Enterococcus faecalis virulence[J]. J Bacteriol, 2012, 194(22): 6066-6073.
[1] Fu Yu, He Wei, Huang Lan. Ferroptosis and its implication in oral diseases [J]. Int J Stomatol, 2024, 51(1): 36-44.
[2] Luo Xiaojie,Wang Dexu,Chen Xiaotao. Relationship between periodontitis and ferroptosis based on bioinformatics analysis [J]. Int J Stomatol, 2023, 50(6): 661-668.
[3] Huang Yuanhong,Peng Xian,Zhou Xuedong.. Progress in research into the effect of Rhizoma Drynariae on the treatment of bone-related diseases in the oral cavity [J]. Int J Stomatol, 2023, 50(6): 679-685.
[4] Hu Jia,Wang Xiuqing,Lu Guoying,Huang Xiaojing.. Regenerative endodontic procedures for permanent tooth with immature apices in adult patients [J]. Int J Stomatol, 2023, 50(6): 686-695.
[5] Gong Meiling,Cheng Xingqun,Wu Hongkun.. Research progress on the correlation between Parkinson’s disease and periodontitis [J]. Int J Stomatol, 2023, 50(5): 587-593.
[6] Sun Jia,Han Ye,Hou Jianxia. Research progress on the role of interleukin-6-hepcidin signal axis in regulating the pathogenesis of periodontitis-associated anemia [J]. Int J Stomatol, 2023, 50(3): 329-334.
[7] Liang Zhiying,Zhao Yuanxi,Zhu Jiani,Su Qin.. Retrospective analysis of clinical data of 288 cases of endodontic microsurgery on anterior teeth [J]. Int J Stomatol, 2023, 50(2): 166-171.
[8] Liu Tiqian,Liang Xing,Liu Weiqing,Li Xiaohong,Zhu Rui.. Research progress on the role and mechanism of occlusal trauma in the development of periodontitis [J]. Int J Stomatol, 2023, 50(1): 19-24.
[9] Li Qiong,Yu Weixian. Research progress on resveratrol for the treatment of periodontitis and its bioavailability [J]. Int J Stomatol, 2023, 50(1): 25-31.
[10] Huang Weikun,Xu Qiuyan,Zhou Ting.. Role of baicalin and mechanisms through which baicalin attenuates oxidative stress injury induced by lipopolysaccharide on macrophages [J]. Int J Stomatol, 2022, 49(5): 521-528.
[11] Zhou Jianpeng,Xie Xudong,Zhao Lei,Wang Jun.. Research progress on the roles and mechanisms of T-helper 17 cells and interleukin-17 in periodontitis [J]. Int J Stomatol, 2022, 49(5): 586-592.
[12] Chen Huiyu,Bai Mingru,Ye Ling.. Progress in understanding the correlations between semaphorin 3A and common oral diseases [J]. Int J Stomatol, 2022, 49(5): 593-599.
[13] Zhou Jiajia,Zhao Lei,Xu Xin. Research progress on the genetic polymorphism of periodontitis [J]. Int J Stomatol, 2022, 49(4): 432-440.
[14] Zhu Jiani,Su Qin. Research status of the use of root canal and periapical microflora in refractory periapical periodontitis [J]. Int J Stomatol, 2022, 49(3): 283-289.
[15] Liu Qianxi,Wu Jiayi,Ren Biao,Huang Ruijie. Research progress on the interactions between Enterococcus faecalis and other oral microorganisms [J]. Int J Stomatol, 2022, 49(3): 290-295.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[2] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[3] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[4] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[5] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[6] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[7] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[8] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[9] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[10] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .