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Molecular biological and immunological analysis for the relationship between periodontal disease and atherosclerosis

Research Project

Project/Area Number 13470462
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Periodontal dentistry
Research InstitutionNiigata University

Principal Investigator

YAMAZAKI Kazuhisa  Niigata University, Graduate school of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (00182478)

Co-Investigator(Kenkyū-buntansha) MURATA Masashi  Niigata University, Medical and Dental Hospital, Assistant, 大学院・医歯学総合病院, 助手 (40303135)
YOSHIE Hiromasa  Niigata University, Graduate school of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (20143787)
Project Period (FY) 2001 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥14,200,000 (Direct Cost: ¥14,200,000)
Fiscal Year 2003: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2002: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 2001: ¥5,300,000 (Direct Cost: ¥5,300,000)
KeywordsPeriodontitis / Atherosclerosis / HSP60 / P.gingivalis / Endothelial cell / Adhesion molecules / Proinflammatory cytokines / P.ging valis / P. gingivalis
Research Abstract

Is has been postulated that periodontal infection may be involved in the initiation and progression of atherosclerosis and subsequent coronary heart disease. Although this concept has been supported by epidemiological case control studies, biological relevance of periodontitis to initiation and progression of atherosclerosis remained unknown. In this research project we analyzed the effects of bacterial antigens and inflammatory cytokines synthesized in the periodontitis lesion on endothelial cell function and the role of humoral and cellular immune responses to bacterial antigen and cross-reactive endogenous antigen on the atherogenesis. Lipopolysaccharide (LPS) and GroEL (HSP60) from Porphyromonas gingivalis (P.gingivalis), a representative periodontopathic bacterium, up-regulated the expression of ICAM-1 and VCAM-a on human coronary arterial endothelial cells. IL-1b and TNF-a, both of which are involved in the tissue destruction seen in periodontitis, also up-regulated the expression of these molecules at concentrations seen in the sera of periodontitis patients. Despite being highly homologous between prokaryotic and eukaryotic cells, HSP60s are strongly immunogenic and are thought to implicate in inflammation as well as the autoimmune diseases. Antibody levels to both human and P.gingivalis HSP60s were the highest in atherosclerosis patients followed by periodontitis patients and healthy subjects. Clonal analysis of the T cells clearly demonstrated the presence of not only human HSP60-but also P.gingivalis GroEL-reactive T-cell populations in the peripheral circulation of atherosclerosis patients. Furthermore, these HSP60-reactive T cells seemed to be present in atherosclerotic lesions in some patients. These results clearly indicate that periodontal infection has the potential to affect human coronary arterial endothelial cells and may contribute to the development of subsequent atherosclerosis.

Report

(4 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • 2001 Annual Research Report
  • Research Products

    (24 results)

All Other

All Publications (24 results)

  • [Publications] Ueki, K.et al.: "Self-heat shock protein 60 induces tumor necrosis factor-α in monocyte-derived macrophage : Possible role in chronic inflammatory periodontal disease."Clin Exp.Immunol.. 127:72-77. 72-77 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamazaki, K.et al.: "Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients."Infect.Immun.. 70. 2492-2501 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Itoh, H.et al.: "Oligoclonal accumulations of T cell clones in gingivitis and periodontitis lesions."Oral Microbiol.Immuno.. 17(5). 324-329 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Oda, T.et al.: "Porphyromonas gingivalis antigen preferentially stimulates T cells to express IL-17 but not receptor activator of NF-κB ligand in vitro."Oral Microbiol.Immunol.. 18(1). 30-36 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamazaki, K.et al.: "Single nucleotide polymorphism in the CD14 promoter and periodontal disease expression in a Japanese population."J.Dent.Res.. 82(8). 612-616 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Shimada, Y.et al.: "Association of Tumor Necrosis Factor Receptor Type 2 +587 Gene Polymorphism with Severe Chronic Periodontitis."J.Clin.Periodontol.. (in press). (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamazaki, K.et al.: "Effect of periodontal treatment on the serum antibody levels to heat shock proteins."Clin Exp Immunol.. 135(3)(in press). 478-482 (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Itagaki, M.et al.: "Lack of association of matrix metalloproteinase-1 and -3 gene promoter polymorphisms in Japanese patients with aggressive periodontitis."J Clin Periodontol.. (in press). (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamazaki, K.et al.: "T cell clonality to Porphyromonas gingivalis and human heat shock protein 60s in oatients with atherosclerosis and periodontitis"Oral Microbiology and Immunology. (in press). (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Itagaki, M., Kubota, T.Shimada, Y., Tai, H., Morozumi, T., Yamazaki, K.: "Lack of association of matrix metalloproteinase-1 and -3 gene Promoter polymorphisms in Japanese patients with aggressive periodontitis."J Clin Periodontol.. (in press). (2004)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamazaki, K., Ohsawa, Y., Itoh, H., Ueki-Maruayama, K., Tabeta, K., Oda, T., Nakajima, T., Yoshie, H., Saito, S., Oguma, F., Kodama, M., Aizawa Y., Seymour, G.J.: "T-cell clonality to Porphyromonas gingivalis and human heat shock protein 60s in patients with atherosclerosis and periodontitis."Oral Microbilol Immunol.. (in press). (2004)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Oda T.et al.: "Porphyromonas gingivalis antigen preferentially stimulates T cells to express IL-17 but not receptor activator of NF-κB ligand in vitro"Oral Microbiology and Immunology. 18・1. 30-36 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Yamazaki K.et al.: "Single-nucleotide polymorphism in the CD14 promoter and periodontal disease expression in a Japanese population"Journal of Dental Research. 82・8. 612-616 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Yamazaki K.et al.: "T cell regulation of the immune response to infection in periodontal disease"Histology and Histopathology. 18・3. 889-896 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Yamazaki K.et al.: "Effect of periodontal treatment on the serum antibody levels to heat shock proteins"Clinical and Experimental Immunology. 135(3). 478-482 (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] Yamazaki K.et al.: "T cell clonality to Porphyromonas gingivalis and human heat shock protein 60s in patients with atherosclerosis and periodontitis"Oral Microbiology and Immunology. (in press). (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] Ueki K., et al.: "Self-heat shock protein 60 induces tumor necrosis factor-a in monocyte-derived macrophage : Possible role in chronic inflammatory periodontal diseases"Clinical and Experimental Immunology. 127・1. 72-77 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Itoh H., et al.: "Oligoclonal accumulations of T-cell clones in gingivitis and periodontitis lesions"Oral Microbiology and Immunology. 17・5. 324-329 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Yamazaki K., et al.: "Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients"Infection and Immunity. 70・5. 2492-2501 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] 多部田康一ほか: "動脈硬化症におけるPorphyromonas Gingivalis GroELに対する免疫応答の解析"Bacterial Adherence & Biofilm. 15. 31-38 (2001)

    • Related Report
      2002 Annual Research Report
  • [Publications] Oda T., et al.: "Porphyromonas gingivalis antigen preferentially stimulates T cells to express IL-17 but not receptor activator of NF-κB ligand in vitro"Oral Microbiology and Immunology. (in press).

    • Related Report
      2002 Annual Research Report
  • [Publications] Yamazaki K: "Elevated proportion of natural killer T cells in periodontitis lesions : a common feature of chronic inflammatory diseases"American Journal of Pathology. 158・4. 1391-1398 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Tabeta K: "Characterization of serum antibody to Actinobacillus actinomycetemcomitans GroEL-like protein in periodontitis patients and healthy subjects"Oral Microbiology and Immunology. 16・5. 290-295 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Ueki K: "Self-heat shock protein 60 induces tumor necrosis factor-α in monocyte-derived macrophage : Possible role in chronic inflammatory periodontal disease"Clinical and Experimental Immunology. (in press).

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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