This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Wang, P.-L. Articles by Ohura, K. Search for Related Content PubMed PubMed Citation Social Bookmarking                         What's this?

PORPHYROMONAS GINGIVALIS LIPOPOLYSACCHARIDE SIGNALING IN GINGIVAL FIBROBLASTS–CD14 AND TOLL-LIKE RECEPTORS

Department of Pharmacology, Osaka Dental University, 8-1 Kuzuhahanazono-cho, Hirakata, Osaka 573-1121, Japan;

Correspondence: ^* corresponding author, wang{at}cc.osaka-dent.ac.jp

Periodontal disease is the major cause of adult tooth loss and is commonly characterized by a chronic inflammation caused by infection of oral bacteria. Porphyromonas gingivalis (P. gingivalis) is one of the suspected periodontopathic bacteria and is frequently isolated from the periodontal pockets of patients with chronic periodontal disease. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Gingival fibroblasts, which are the major constituents of gingival connective tissue, may directly interact with bacteria and bacterial products, including LPS, in periodontitis lesions. It is suggested that gingival fibroblasts play an important role in the host responses to LPS in periodontal disease. P. gingivalis LPS enhances the production of inflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor alpha (TNF-) in gingival fibroblasts. However, the receptor that binds with P. gingivalis LPS on gingival fibroblasts remained unknown for many years. Recently, it was demonstrated that P. gingivalis LPS binds to gingival fibroblasts. It was also found that gingival fibroblasts express CD14, Toll-like receptor 4 (TLR4), and myeloid differentiation primary response gene 88 (MyD88). P. gingivalis LPS treatment of gingival fibroblasts activates several intracellular proteins, including protein tyrosine kinases, and up-regulates the expression of monocyte chemoattractant protein-1 (MCP-1), extracellular signal-regulated kinase 1 (ERK1), and signal-regulated kinase 2 (ERK2), IL-1 receptor-associated kinase (IRAK), nuclear factor-B (NF-B), and activating protein-1 (AP-1). These results suggest that the binding of P. gingivalis LPS to CD14 and TLR4 on gingival fibroblasts activates various second-messenger systems. In this article, we review recent findings on the signaling pathways induced by the binding of P. gingivalis LPS to CD14 and Toll-like receptors (TLRs) in gingival fibroblasts.

Key Words: Porphyromonas gingivalis • lipopolysaccharide • gingival fibroblasts • CD14 • Toll-like receptors

Critical Reviews in Oral Biology & Medicine, Vol. 13, No. 2, 132-142 (2002)
DOI: 10.1177/154411130201300204


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				L. Kocgozlu, R. Elkaim, H. Tenenbaum, and S. Werner Variable Cell Responses to P. gingivalis Lipopolysaccharide Journal of Dental Research, August 1, 2009; 88(8): 741 - 745. [Abstract] [Full Text] [PDF]

				S. Kang, S.-P. Lee, K. E. Kim, H.-Z. Kim, S. Memet, and G. Y. Koh Toll-like receptor 4 in lymphatic endothelial cells contributes to LPS-induced lymphangiogenesis by chemotactic recruitment of macrophages Blood, March 12, 2009; 113(11): 2605 - 2613. [Abstract] [Full Text] [PDF]

				D. J. Davidson, A. J. Currie, D. M. E. Bowdish, K. L. Brown, C. M. Rosenberger, R. C. Ma, J. Bylund, P. A. Campsall, A. Puel, C. Picard, et al. IRAK-4 Mutation (Q293X): Rapid Detection and Characterization of Defective Post-Transcriptional TLR/IL-1R Responses in Human Myeloid and Non-Myeloid Cells J. Immunol., December 1, 2006; 177(11): 8202 - 8211. [Abstract] [Full Text] [PDF]

				R. P. Darveau, T.-T. T. Pham, K. Lemley, R. A. Reife, B. W. Bainbridge, S. R. Coats, W. N. Howald, S. S. Way, and A. M. Hajjar Porphyromonas gingivalis Lipopolysaccharide Contains Multiple Lipid A Species That Functionally Interact with Both Toll-Like Receptors 2 and 4 Infect. Immun., September 1, 2004; 72(9): 5041 - 5051. [Abstract] [Full Text] [PDF]

				S. R. Coats, R. A. Reife, B. W. Bainbridge, T.-T. T. Pham, and R. P. Darveau Porphyromonas gingivalis Lipopolysaccharide Antagonizes Escherichia coli Lipopolysaccharide at Toll-Like Receptor 4 in Human Endothelial Cells Infect. Immun., December 1, 2003; 71(12): 6799 - 6807. [Abstract] [Full Text] [PDF]

				X. Li, L. Wang, D.P. Nunes, R.F. Troxler, and G.D. Offner Pro-inflammatory Cytokines Up-regulate MUC1 Gene Expression in Oral Epithelial Cells Journal of Dental Research, November 1, 2003; 82(11): 883 - 887. [Abstract] [Full Text] [PDF]

				G. Hajishengallis, M. Martin, R. E. Schifferle, and R. J. Genco Counteracting Interactions between Lipopolysaccharide Molecules with Differential Activation of Toll-Like Receptors Infect. Immun., December 1, 2002; 70(12): 6658 - 6664. [Abstract] [Full Text] [PDF]