粪肠球菌在难治性根尖周炎炎症反应中的研究进展
Research Progress of Enterococcus faecalis in Inflammatory Response in Refractory Apical Periodontitis
DOI: 10.12677/ACM.2023.13122752, PDF,    科研立项经费支持
作者: 关 镕:新疆医科大学研究生院,新疆 乌鲁木齐 ;赵 莉*, 马依热·阿布都赛麦提:新疆维吾尔自治区人民医院口腔科,新疆 乌鲁木齐
关键词: 粪肠球菌难治性根尖周炎持续性根尖周炎脂磷壁酸巨噬细胞IL-1IL-1βTreg细胞Enterococcus faecalis Refractory Apical Periodontitis Persistent Apical Periodontitis Lipoteichoic Acid Macrophages IL-1 IL-1β Treg Cells
摘要: 粪肠球菌作为难治性根尖周炎的主要致病菌,能够在恶劣环境中形成粘附力极强的生物膜而长期生存,对氢氧化钙等根管消毒药物和机械清理具有抵抗性,是感染根管治疗失败的主要原因。因此,粪肠球菌已成为牙髓病学领域最近的研究重点。粪肠球菌的致病性主要表现在细菌侵入根尖周组织后激活机体免疫反应,激活RIPK3/MLKL信号通路并诱导巨噬细胞凋亡从而分泌细胞因子发挥抗炎和抑炎作用,造成根尖周组织的持续炎症,也会引发全身多种器官感染。本文就粪肠球菌在难治性根尖周炎中的致病性相关机制做一综述。
Abstract: As the main pathogenic bacteria in the root canal of refractory apical periodontitis, Enterococcus faecalis can survive for a long time in harsh environments to form biofilms with strong adhesion, and is resistant to root canal disinfection drugs such as calcium hydroxide and mechanical cleaning, which is the main reason for the failure of infection root canal treatment. The pathogenicity of En-terococcus faecalis is mainly manifested in the activation of the body’s immune response after the bacteria invade the periapical tissue, initiating the Th17/Treg cell pathway and inducing apoptosis of macrophages to secrete cytokines to exert anti-inflammatory and anti-inflammatory effects, re-sulting in continuous inflammation of periapical tissues, and eventually causing multiple organ in-fections throughout the body. This article reviews the pathogenicity-related mechanism of Entero-coccus faecalis in refractory apical periodontitis.
文章引用:关镕, 赵莉, 马依热·阿布都赛麦提. 粪肠球菌在难治性根尖周炎炎症反应中的研究进展[J]. 临床医学进展, 2023, 13(12): 19547-19553. https://doi.org/10.12677/ACM.2023.13122752

参考文献

[1] Ali, I.A.A., Cheung, G.S.P. and Neelakantan, P. (2022) Transition Metals and Enterococcus faecalis: Homeostasis, Vir-ulence and Perspectives. Molecular Oral Microbiology, 37, 276-291. [Google Scholar] [CrossRef] [PubMed]
[2] Gaca, A.O. and Lemos, J.A. (2019) Adaptation to Adversity: The Intermingling of Stress Tolerance and Pathogenesis in Enter-ococci. Microbiology and Molecular Biology Reviews, 83, e00008-19. [Google Scholar] [CrossRef
[3] Da, S.R., Tay, W.H., Ho, F.K., et al. (2022) Enterococcus faecalis Alters Endo-Lysosomal Trafficking to Replicate and Persist within Mammalian Cells. PLOS Pathogens, 18, e1010434. [Google Scholar] [CrossRef] [PubMed]
[4] Ch’Ng, J.H., Chong, K., Lam, L.N., et al. (2019) Bio-film-Associated Infection by Enterococci. Nature Reviews Microbiology, 17, 82-94. [Google Scholar] [CrossRef] [PubMed]
[5] Deng, Z., Lin, B., Liu, F., et al. (2023) Role of Enterococcus fae-calis in Refractory Apical Periodontitis: From Pathogenicity to Host Cell Response. Journal of Oral Microbiology, 15, Article ID: 2184924. [Google Scholar] [CrossRef] [PubMed]
[6] Wu, S., Liu, Y., Zhang, H., et al. (2020) Nano-Graphene Oxide with Antisense walR RNA Inhibits the Pathogenicity of Enterococcus faecalis in Periapical Periodontitis. Journal of Dental Sciences, 15, 65-74. [Google Scholar] [CrossRef] [PubMed]
[7] Jia, G., Yu, M., Shang, X.H., et al. (2021) A Five-Year Experience for Treating Patients with Chronic Apical Periodontitis with Root Canal Treatment: A Retrospective Cohort Study. Shanghai Journal of Stomatology, 30, 124-128.
[8] Siqueira, J.F., Antunes, H.S., Pérez, A.R., et al. (2020) The Apical Root Canal System of Teeth with Posttreatment Apical Periodontitis: Correlating Microbiologic, Tomographic, and His-topathologic Findings. Journal of Endodontics, 46, 1195-1203. [Google Scholar] [CrossRef] [PubMed]
[9] Hu, T., Lei, L. and Zhou, X.D. (2022) Research Progress in Pathogenesis and Control of Enterococcus faecalis with Persis-tent Infection in Root Canals. Chinese Journal of Stomatology, 57, 10-15.
[10] Daw, K., Baghdayan, A.S., Awasthi, S., et al. (2012) Biofilm and Planktonic Enterococcus faecalis Elicit Different Responses from Host Phagocytes in Vitro. FEMS Immunology and Medical Microbiology, 65, 270-282. [Google Scholar] [CrossRef
[11] Elashiry, M.M., Elashiry, M., Zeitoun, R., et al. (2020) Enterococcus faecalis Induces Differentiation of Immune-Aberrant Dendritic Cells from Murine Bone Marrow-Derived Stem Cells. Infection and Immunity, 88, e00338-20. [Google Scholar] [CrossRef
[12] Gomes, B.P.F.A., Francisco, P.A., Godoi Jr., E.P., et al. (2021) Identi-fication of Culturable and Nonculturable Microorganisms, Lipopolysaccharides, and Lipoteichoic Acids from Root Ca-nals of Teeth with Endodontic Failure. Journal of Endodontics, 47, 1075-1086. [Google Scholar] [CrossRef] [PubMed]
[13] Wang, L., Jin, H., Ao, X., et al. (2019) JAK2-STAT3 Signaling Pathway Is Involved in Rat Periapical Lesions Induced by Enterococcus faecalis. Oral Diseases, 25, 1769-1779. [Google Scholar] [CrossRef] [PubMed]
[14] Lima, S.M., Sousa, M.G., Freire, M.S., et al. (2015) Immune Response Profile against Persistent Endodontic Pathogens Candida albicans and Enterococcus faecalis in Vitro. Journal of Endo-dontics, 41, 1061-1065. [Google Scholar] [CrossRef] [PubMed]
[15] Kowalski, W.J., Kasper, E.L., Hatton, J.F., et al. (2006) Entero-coccus faecalis Adhesin, Ace, Mediates Attachment to Particulate Dentin. Journal of Endodontics, 32, 634-637. [Google Scholar] [CrossRef] [PubMed]
[16] Guneser, M.B. and Eldeniz, A.U. (2016) The Effect of Gelatinase Production of Enterococcus faecalis on Adhesion to Dentin after Irrigation with Various Endodontic Irrigants. Acta Bio-materialia Odontologica Scandinavica, 2, 144-149. [Google Scholar] [CrossRef] [PubMed]
[17] 郭惠杰, 岳林. 粪肠球菌在根管内定植模式的体外研究[J]. 北京大学学报(医学版), 2009, 41(6): 699-701.
[18] Su, C., Zhang, R., Wang, R., et al. (2022) Prognostic Predic-tors of Endodontic Microsurgery: Radiographic Assessment. International Dental Journal, 72, 628-633. [Google Scholar] [CrossRef] [PubMed]
[19] Xu, Z., Tong, Z., Neelakantan, P., et al. (2018) Enterococcus fae-calis Immunoregulates Osteoclastogenesis of Macrophages. Experimental Cell Research, 362, 152-158. [Google Scholar] [CrossRef] [PubMed]
[20] Van Hoecke, L., Van Lint, S., Roose, K., et al. (2018) Treatment with mRNA Coding for the Necroptosis Mediator MLKL Induces Antitumor Immunity Directed against Neo-Epitopes. Nature Communications, 9, Article No. 3417. [Google Scholar] [CrossRef] [PubMed]
[21] Dai, X., Ma, R., Jiang, W., et al. (2022) Enterococcus faecal-is-Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis. Microbiology Spectrum, 10, e104522. [Google Scholar] [CrossRef] [PubMed]
[22] Dai, X., Deng, Z., Liang, Y., et al. (2020) Enterococcus faecalis Induces Necroptosis in Human Osteoblastic MG63 Cells through the RIPK3/MLKL Signalling Pathway. International Endodontic Journal, 53, 1204-1215. [Google Scholar] [CrossRef] [PubMed]
[23] Fu, Q., Chen, K., Zhu, Q., et al. (2017) Beta-Catenin Promotes Intracellular Bacterial Killing via Suppression of Pseudomonas aeruginosa-Triggered Macrophage Autophagy. Journal of Interna-tional Medical Research, 45, 556-569. [Google Scholar] [CrossRef] [PubMed]
[24] Lin, D., Gao, Y., Zhao, L., et al. (2018) Enterococcus faecalis Lipoteichoic Acid Regulates Macrophages Autophagy via PI3K/Akt/mTOR Pathway. Biochemical and Biophysical Re-search Communications, 498, 1028-1036. [Google Scholar] [CrossRef] [PubMed]
[25] Zhai, C., Cheng, J., Mujahid, H., et al. (2014) Selective Inhibition of PI3K/Akt/mTOR Signaling Pathway Regulates Autophagy of Macrophage and Vulnerability of Atherosclerotic Plaque. PLOS ONE, 9, e0090563. [Google Scholar] [CrossRef] [PubMed]
[26] 陈宇雄, 杨詠嘉, 黄元瑾. IL-1β和TNF-α对成骨样MG63细胞OPG和RANKL表达的影响[J]. 广东医学, 2018, 39(16): 2414-2418.
[27] Tazawa, K., Azuma, P.M., Furusho, H., et al. (2022) Revisiting the Role of IL-1 Signaling in the Development of Apical Periodontitis. Frontiers in Dental Medicine, 3, Article ID: 985558. [Google Scholar] [CrossRef] [PubMed]
[28] Matsuo, T., Ebisu, S., Nakanishi, T., et al. (1994) Interleukin-1 alpha and Interleukin-1 beta Periapical Exudates of Infected Root Canals: Correlations with the Clinical Findings of the Involved Teeth. Journal of Endodontics, 20, 432-435. [Google Scholar] [CrossRef
[29] Eislmayr, K., Bestehorn, A., Morelli, L., et al. (2022) Non-redundancy of IL-1alpha and IL-1beta Is Defined by Distinct Regulation of Tissues Orchestrating Resistance versus Tol-erance to Infection. Science Advances, 8, eabj7293. [Google Scholar] [CrossRef] [PubMed]
[30] 樊佳, 赵二川, 叶震璇, 等. ASC与Caspase-1在PBC患者外周血中的表达研究[J]. 重庆医学, 2018, 47(8): 1044-1048.
[31] Ran, S., Huang, J., Liu, B., et al. (2021) Enterococcus faecalis Activates NLRP3 Inflammasomes Leading to Increased Interleukin-1 beta Secretion and Pyroptosis of THP-1 Macrophages. Microbial Pathogenesis, 154, Article ID: 104761. [Google Scholar] [CrossRef] [PubMed]
[32] Lu, B., Zhang, J., Huang, X., et al. (2015) Expression of Inter-leukin-1beta and Matrix Metalloproteinase-8 in Cytolytic and Noncytolytic Enterococcus faecalis-Induced Persistent Ap-ical Periodontitis: A Comparative Study in the Rat. Journal of Endodontics, 41, 1288-1293. [Google Scholar] [CrossRef] [PubMed]
[33] Istomine, R., Pavey, N. and Piccirillo, C.A. (2016) Posttranscrip-tional and Translational Control of Gene Regulation in CD4+ T Cell Subsets. The Journal of Immunology, 196, 533-540. [Google Scholar] [CrossRef] [PubMed]
[34] Sakaguchi, S., Mikami, N., Wing, J.B., et al. (2020) Regulatory T Cells and Human Disease. Annual Review of Immunology, 38, 541-566. [Google Scholar] [CrossRef] [PubMed]
[35] 李梦菲, 仉红, 赵少剑, 等. 叉头样转录因子3在粪肠球菌感染模型大鼠难治性根尖周炎病变中的表达[J]. 中国组织工程研究, 2023, 27(8): 1187-1192.
[36] Li, R., Hu, Y. and Hou, S. (2022) An Exploration of Oral-Gut Pathogens Mediating Immune Escape of Pancreatic Cancer via miR-21/PTEN Axis. Frontiers in Microbiology, 13, Article ID: 928846. [Google Scholar] [CrossRef] [PubMed]