This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoshimura, A.
Right arrow Articles by Hara, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoshimura, A.
Right arrow Articles by Hara, Y.

 Previous Article  |  Next Article 

Infection and Immunity, January 2002, p. 218-225, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.218-225.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Lipopolysaccharides from Periodontopathic Bacteria Porphyromonas gingivalis and Capnocytophaga ochracea Are Antagonists for Human Toll-Like Receptor 4

Atsutoshi Yoshimura,1* Takashi Kaneko,1 Yoshifumi Kato,1 Douglas T. Golenbock,2 and Yoshitaka Hara1

Department of Periodontology, Nagasaki University School of Dentistry, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan,1 Department of Medicine, Division of Infectious Diseases, University of Massachusetts Medical School, Worcester, Massachusetts 016552

Received 1 March 2001/ Returned for modification 7 May 2001/ Accepted 9 October 2001

Toll-like receptors (TLRs) 2 and 4 have recently been identified as possible signal transducers for various bacterial ligands. To investigate the roles of TLRs in the recognition of periodontopathic bacteria by the innate immune system, a Chinese hamster ovary (CHO) nuclear factor-{kappa}B (NF-{kappa}B)-dependent reporter cell line, 7.7, which is defective in both TLR2- and TLR4-dependent signaling pathways was transfected with human CD14 and TLRs. When the transfectants were exposed to freeze-dried periodontopathic bacteria, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Capnocytophaga ochracea, and Fusobacterium nucleatum, and a non-oral bacterium, Escherichia coli, all species of the bacteria induced NF-{kappa}B-dependent CD25 expression in 7.7/huTLR2 cells. Although freeze-dried A. actinomycetemcomitans, F. nucleatum, and E. coli also induced CD25 expression in 7.7/huTLR4 cells, freeze-dried P. gingivalis did not. Similarly, lipopolysaccharides (LPS) extracted from A. actinomycetemcomitans, F. nucleatum, and E. coli induced CD25 expression in 7.7/huTLR4 cells, but LPS from P. gingivalis and C. ochracea did not. Furthermore, LPS from P. gingivalis and C. ochracea attenuated CD25 expression in 7.7/huTLR4 cells induced by repurified LPS from E. coli. LPS from P. gingivalis and C. ochracea also inhibited the secretion of interleukin-6 (IL-6) from U373 cells, the secretion of IL-1ß from human peripheral blood mononuclear cells, and ICAM-1 expression in human gingival fibroblasts induced by repurified LPS from E. coli. These findings indicated that LPS from P. gingivalis and C. ochracea worked as antagonists for human TLR4. The antagonistic activity of LPS from these periodontopathic bacteria may be associated with the etiology of periodontal diseases.

* Corresponding author. Mailing address: Department of Periodontology, Nagasaki University School of Dentistry, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan. Phone: 81-95-849-7683. Fax: 81-95-849-7684. E-mail: ayoshi{at}net.nagasaki-u.ac.jp.

Editor: R. N. Moore

Infection and Immunity, January 2002, p. 218-225, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.218-225.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Gaffen, S.L., Hajishengallis, G. (2008). A New Inflammatory Cytokine on the Block: Re-thinking Periodontal Disease and the Th1/Th2 Paradigm in the Context of Th17 Cells and IL-17. JDR 87: 817-828 [Abstract] [Full Text]  
  • Jemmett, K., Macagno, A., Molteni, M., Heckels, J. E., Rossetti, C., Christodoulides, M. (2008). A Cyanobacterial Lipopolysaccharide Antagonist Inhibits Cytokine Production Induced by Neisseria meningitidis in a Human Whole-Blood Model of Septicemia. Infect. Immun. 76: 3156-3163 [Abstract] [Full Text]  
  • Rangarajan, M., Aduse-Opoku, J., Paramonov, N., Hashim, A., Bostanci, N., Fraser, O. P., Tarelli, E., Curtis, M. A. (2008). Identification of a Second Lipopolysaccharide in Porphyromonas gingivalis W50. J. Bacteriol. 190: 2920-2932 [Abstract] [Full Text]  
  • Handfield, M., Baker, H.V., Lamont, R.J. (2008). Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells. JDR 87: 203-223 [Abstract] [Full Text]  
  • Zhou, Q., Amar, S. (2007). Identification of Signaling Pathways in Macrophage Exposed to Porphyromonas gingivalis or to Its Purified Cell Wall Components. J. Immunol. 179: 7777-7790 [Abstract] [Full Text]  
  • Popa, C., Abdollahi-Roodsaz, S., Joosten, L. A. B., Takahashi, N., Sprong, T., Matera, G., Liberto, M. C., Foca, A., van Deuren, M., Kullberg, B. J., van den Berg, W. B., van der Meer, J. W. M., Netea, M. G. (2007). Bartonella quintana Lipopolysaccharide Is a Natural Antagonist of Toll-Like Receptor 4. Infect. Immun. 75: 4831-4837 [Abstract] [Full Text]  
  • Mahanonda, R., Sa-Ard-Iam, N., Montreekachon, P., Pimkhaokham, A., Yongvanichit, K., Fukuda, M. M., Pichyangkul, S. (2007). IL-8 and IDO Expression by Human Gingival Fibroblasts via TLRs. J. Immunol. 178: 1151-1157 [Abstract] [Full Text]  
  • Macagno, A., Molteni, M., Rinaldi, A., Bertoni, F., Lanzavecchia, A., Rossetti, C., Sallusto, F. (2006). A cyanobacterial LPS antagonist prevents endotoxin shock and blocks sustained TLR4 stimulation required for cytokine expression. JEM 203: 1481-1492 [Abstract] [Full Text]  
  • Fujimura, Y., Hotokezaka, H., Ohara, N., Naito, M., Sakai, E., Yoshimura, M., Narita, Y., Kitaura, H., Yoshida, N., Nakayama, K. (2006). The Hemoglobin Receptor Protein of Porphyromonas gingivalis Inhibits Receptor Activator NF-{kappa}B Ligand-Induced Osteoclastogenesis from Bone Marrow Macrophages.. Infect. Immun. 74: 2544-2551 [Abstract] [Full Text]  
  • Brozovic, S., Sahoo, R., Barve, S., Shiba, H., Uriarte, S., Blumberg, R. S., Kinane, D. F. (2006). Porphyromonas gingivalis enhances FasL expression via up-regulation of NF{kappa}B-mediated gene transcription and induces apoptotic cell death in human gingival epithelial cells.. Microbiology 152: 797-806 [Abstract] [Full Text]  
  • Teng, Y.-T.A. (2006). Protective and Destructive Immunity in the Periodontium: Part 1--Innate and Humoral Immunity and the Periodontium. JDR 85: 198-208 [Abstract] [Full Text]  
  • Lee, S.-H., Kim, K.-K., Rhyu, I.-C., Koh, S., Lee, D.-S., Choi, B.-K. (2006). Phenol/water extract of Treponema socranskii subsp. socranskii as an antagonist of Toll-like receptor 4 signalling. Microbiology 152: 535-546 [Abstract] [Full Text]  
  • Coats, S. R., Pham, T.-T. T., Bainbridge, B. W., Reife, R. A., Darveau, R. P. (2005). MD-2 Mediates the Ability of Tetra-Acylated and Penta-Acylated Lipopolysaccharides to Antagonize Escherichia coli Lipopolysaccharide at the TLR4 Signaling Complex. J. Immunol. 175: 4490-4498 [Abstract] [Full Text]  
  • Kikuchi, T., Willis, D.L., Liu, M., Purkall, D.B., Sukumar, S., Barbour, S.E., Schenkein, H.A., Tew, J.G. (2005). Dendritic-NK Cell Interactions in P. gingivalis-specific Responses. JDR 84: 858-862 [Abstract] [Full Text]  
  • Hunstad, D. A., Justice, S. S., Hung, C. S., Lauer, S. R., Hultgren, S. J. (2005). Suppression of Bladder Epithelial Cytokine Responses by Uropathogenic Escherichia coli. Infect. Immun. 73: 3999-4006 [Abstract] [Full Text]  
  • Asai, Y., Hashimoto, M., Fletcher, H. M., Miyake, K., Akira, S., Ogawa, T. (2005). Lipopolysaccharide Preparation Extracted from Porphyromonas gingivalis Lipoprotein-Deficient Mutant Shows a Marked Decrease in Toll-Like Receptor 2-Mediated Signaling. Infect. Immun. 73: 2157-2163 [Abstract] [Full Text]  
  • Takii, R., Kadowaki, T., Baba, A., Tsukuba, T., Yamamoto, K. (2005). A Functional Virulence Complex Composed of Gingipains, Adhesins, and Lipopolysaccharide Shows High Affinity to Host Cells and Matrix Proteins and Escapes Recognition by Host Immune Systems. Infect. Immun. 73: 883-893 [Abstract] [Full Text]  
  • Darveau, R. P., Pham, T.-T. T., Lemley, K., Reife, R. A., Bainbridge, B. W., Coats, S. R., Howald, W. N., Way, S. S., Hajjar, A. M. (2004). Porphyromonas gingivalis Lipopolysaccharide Contains Multiple Lipid A Species That Functionally Interact with Both Toll-Like Receptors 2 and 4. Infect. Immun. 72: 5041-5051 [Abstract] [Full Text]  
  • Kikuchi, T., Hahn, C. L., Tanaka, S., Barbour, S. E., Schenkein, H. A., Tew, J. G. (2004). Dendritic Cells Stimulated with Actinobacillus actinomycetemcomitans Elicit Rapid Gamma Interferon Responses by Natural Killer Cells. Infect. Immun. 72: 5089-5096 [Abstract] [Full Text]  
  • Coats, S. R., Reife, R. A., Bainbridge, B. W., Pham, T.-T. T., Darveau, R. P. (2003). Porphyromonas gingivalis Lipopolysaccharide Antagonizes Escherichia coli Lipopolysaccharide at Toll-Like Receptor 4 in Human Endothelial Cells. Infect. Immun. 71: 6799-6807 [Abstract] [Full Text]  
  • Murray, D. A, Wilton, J. M. A. (2003). Lipopolysaccharide from the Periodontal Pathogen Porphyromonas gingivalis Prevents Apoptosis of HL60-Derived Neutrophils In Vitro. Infect. Immun. 71: 7232-7235 [Abstract] [Full Text]  
  • LeClair, E.E. (2003). Four Reasons to Consider a Novel Class of Innate Immune Molecules in the Oral Epithelium. JDR 82: 944-950 [Abstract] [Full Text]  
  • Hajishengallis, G., Martin, M., Schifferle, R. E., Genco, R. J. (2002). Counteracting Interactions between Lipopolysaccharide Molecules with Differential Activation of Toll-Like Receptors. Infect. Immun. 70: 6658-6664 [Abstract] [Full Text]  
  • HENDERSON, B., WILSON, M., SHARP, L., WARD, J. M. (2002). Actinobacillus actinomycetemcomitans. J Med Microbiol 51: 1013-1020 [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»