成牙本质细胞在牙髓免疫反应中作用的研究进展

摘要/Abstract

摘要： 深龋时龋病相关细菌侵入牙本质深层接近牙髓，成牙本质细胞层位于牙髓牙本质交界处，作为牙髓组织最先接触外源性刺激的第一道防线，可通过模式识别受体（PRRs，如Toll样受体、天然免疫受体NOD）识别多种病原相关分子模式（PAMPs），产生促炎细胞因子、表达细胞粘附分子，启动免疫应答。多种细胞因子、细胞粘附分子参与牙髓炎的发生。本文就成牙本质细胞通过TLRs、NLRs识别细菌性因素、引起牙髓免疫反应导致牙髓炎过程中的作用及其研究进展作一综述。

关键词: 成牙本质细胞，Toll样受体，Nod样受体，牙髓炎

Abstract: Abstract：In deep dental caries, as caries-related bacteria invade into dentinal tubules and come close to the pulp, odontoblasts, which are situated at the pulp-dentin interface and function as the first defense line toward cariogenic bacteria, can sense bacteria via pattern recognition receptors (PRRs, including Toll-like receptors and nucleotide-binding oligomerization domain) for different pathogen-associated molecular patterns (PAMPs), produce proinflammatory cytokines, express cell adhesion molecules, and initiate innate immune responses. Many kinds of cytokines and adhesion molecules are involved in the initiation and development of pulpitis. This article reviews the research progress on how odontoblasts recognize bacterium-related factors via TLRs and NODs, cause pulp immune responses and function in subsequent pulpitis.

Key words: Odontoblast，Toll-like receptor(TLR)，Nod-like receptor，Pulpitis

中图分类号:

R780.2

胡琛马瑞阳. 成牙本质细胞在牙髓免疫反应中作用的研究进展[J]. , 2015, 35(10): 893-873.

参考文献

Iwasaki A, Medzhitov R. Regulation of adaptive immunity by the innate immune system[J]. Science, 2010, 327(5963): 291-295.
Cooper P R, Smith A J. Molecular mediators of pulp inflammation and regeneration[J]. Endodontic Topics, 2013, 28(1): 90-105.
Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity[J]. Cell, 2006, 124(4): 783-801.
Beutler B A. TLRs and innate immunity[J]. Blood, 2009, 113(7): 1399-1407.
Staquet M J, Durand S H, Colomb E, et al. Different roles of odontoblasts and fibroblasts in immunity[J]. Journal of dental research, 2008, 87(3): 256-261.
Carrouel F, Staquet M J, Keller J F, et al. Lipopolysaccharide-binding protein inhibits toll-like receptor 2 activation by lipoteichoic acid in human odontoblast-like cells[J]. Journal of endodontics, 2013, 39(8): 1008-1014.
Tapping R I, Akashi S, Miyake K, et al. Toll-like receptor 4, but not toll-like receptor 2, is a signaling receptor for Escherichia and Salmonella lipopolysaccharides[J]. The Journal of Immunology, 2000, 165(10): 5780-5787.
Akira S, Takeda K. Toll-like receptor signalling[J]. Nature Reviews Immunology, 2004, 4(7): 499-511.
Kawai T, Akira S. Pathogen recognition with Toll-like receptors[J]. Current opinion in immunology, 2005, 17(4): 338-344.
Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors[J]. Nature immunology, 2010, 11(5): 373-384.
Chen G, Shaw M H, Kim Y G, et al. NOD-like receptors: role in innate immunity and inflammatory disease[J]. Annual Review of Pathological Mechanical Disease, 2009, 4: 365-398.
Lee Y Y, Chan C H, Hung S L, et al. Up-regulation of nucleotide-binding oligomerization domain 1 in inflamed human dental pulp[J]. Journal of endodontics, 2011, 37(10): 1370-1375.
Jiang H W, Zhang W, Ren B P, et al. Expression of toll like receptor 4 in normal human odontoblasts and dental pulp tissue[J]. Journal of endodontics, 2006, 32(8): 747-751.
Veerayutthwilai O, Byers M R, Pham T T T, et al. Differential regulation of immune responses by odontoblasts[J]. Oral microbiology and immunology, 2007, 22(1): 5-13.
Abreu M T, Fukata M, Arditi M. TLR signaling in the gut in health and disease[J]. The Journal of Immunology, 2005, 174(8): 4453-4460.
Takeda K, Akira S. Toll-like receptors in innate immunity[J]. International immunology, 2005, 17(1): 1-14.
Love R M, Jenkinson H F. Invasion of dentinal tubules by oral bacteria[J]. Critical Reviews in Oral Biology & Medicine, 2002, 13(2): 171-183.
Tronstad L. Clinical endodontics: a textbook[M]. Thieme, 2009.
Lili H, Qianying K, Xi W. Toll-like receptor's role in intracellular signal pathways and its immune adjustment function[J]. International Journal of Stomatology, 2013, 1: 025.
Farges J C, Carrouel F, Keller J F, et al. Cytokine production by human odontoblast-like cells upon Toll-like receptor-2 engagement[J]. Immunobiology, 2011, 216(4): 513-517.
Durand S H, Flacher V, Roméas A, et al. Lipoteichoic acid increases TLR and functional chemokine expression while reducing dentin formation in in vitro differentiated human odontoblasts[J]. The Journal of Immunology, 2006, 176(5): 2880-2887.
Keller J F, Carrouel F, Colomb E, et al. Toll-like receptor 2 activation by lipoteichoic acid induces differential production of pro-inflammatory cytokines in human odontoblasts, dental pulp fibroblasts and immature dendritic cells[J]. Immunobiology, 2010, 215(1): 53-59.
Horst O V, Tompkins K A, Coats S R, et al. TGF-β1 inhibits TLR-mediated odontoblast responses to oral bacteria[J]. Journal of dental research, 2009, 88(4): 333-338.
Mutoh N, Tani-Ishii N, Tsukinoki K, et al. Expression of toll-like receptor 2 and 4 in dental pulp[J]. Journal of endodontics, 2007, 33(10): 1183-1186.
Staquet M J, Durand S H, Colomb E, et al. Different roles of odontoblasts and fibroblasts in immunity[J]. Journal of dental research, 2008, 87(3): 256-261.
Lee Y Y, Chan C H, Hung S L, et al. Up-regulation of nucleotide-binding oligomerization domain 1 in inflamed human dental pulp[J]. Journal of endodontics, 2011, 37(10): 1370-1375.
Lin Z M, Song Z, Qin W, et al. Expression of nucleotide-binding oligomerization domain 2 in normal human dental pulp cells and dental pulp tissues[J]. Journal of endodontics, 2009, 35(6): 838-842.
Keller J F, Carrouel F, Staquet M J, et al. Expression of NOD2 is increased in inflamed human dental pulps and lipoteichoic acid-stimulated odontoblast-like cells[J]. Innate immunity, 2011, 17(1): 29-34.
Hirao K, Yumoto H, Takahashi K, et al. Roles of TLR2, TLR4, NOD2, and NOD1 in pulp fibroblasts[J]. Journal of dental research, 2009, 88(8): 762-767.
Yang C S, Shin D M, Jo E K. The role of NLR-related protein 3 inflammasome in host defense and inflammatory diseases[J]. International neurourology journal, 2012, 16(1): 2-12.
Song Z, Lin Z, He F, et al. NLRP3 is expressed in human dental pulp cells and tissues[J]. Journal of endodontics, 2012, 38(12): 1592-1597.
Hirao K, Yumoto H, Nakanishi T, et al. Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells[J]. Life sciences, 2010, 86(17): 654-660.
Nakanishi T, Mukai K, Yumoto H, et al. Anti‐inflammatory effect of catechin on cultured human dental pulp cells affected by bacteria‐derived factors[J]. European journal of oral sciences, 2010, 118(2): 145-150. Nakanishi T, Mukai K, Yumoto H, et al. Anti‐inflammatory effect of catechin on cultured human dental pulp cells affected by bacteria‐derived factors[J]. European journal of oral sciences, 2010, 118(2): 145-150.

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