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Elucidation of developing mechanisms for infectious endocarditis using a proteomic technique

Research Project

Project/Area Number 14571953
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 矯正・小児・社会系歯学
Research InstitutionKyushu University

Principal Investigator

YAMAGUCHI Noboru  Kyushu University, Faculty of Dental Science, Preventive Dentistry, Instructor, 歯学研究院, 助手 (00230368)

Co-Investigator(Kenkyū-buntansha) MASUHIRO Yoshikazu  Instructor, Faculty of Dental Science, Oral Infectious Diseases & Immunolgy, Instructor, 歯学研究院, 助手 (00336083)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
Keywordsperiodontopathic bacteria / human endothelial cell / proteomics / inflammatory cytokine / leukotoxin / apoptosis / integrin / caspase
Research Abstract

First of all, to elucidate the developing mechanisms for infectious endocarditis, we analyzed some proteins which are induced and produced from human endothelial cells (EA.hy926) infected with Acanobacillus acdnornycetemcomians (Aa) strain SUNY465 using a proteomic technique. This result suggested that several inflammatory cytokines might be induced after the bacterial invasion to the cell. We demonstrated previously that Aa leukotoxin (Ltx) is strongly able to induce apoptotic signal of cells that are positive for lymphocyte function-associated antigen-1 (LFA-1), a cell receptor of Ltx. So we next investigated whether inflammatory cytokines regulate apoptosis of human leukemic HL-60 cells induced by the Ltx. Of these cytokines tested, TNF-α, IL-1α and IL-1β significantly enhanced the Ltx-induced cell apoptosis. Northern and Western blotting analyses showed that TNF-a enhanced the expression of CD11a in the cells at mRNA and protein level, but did not for CD18. TNF-α also enhanced the binding of Ltx to the cells. We also observed by measuring mitochondrial transmembrane potential and the generation of superoxide. anion that the cytokine enhanced Ltx-induced HL-60 cell apoptosis. The enhancing action was strongly neutralized by anti-TNF-receptor 1 antibody, though anti-TNF-receptor 2 antibody did not so. In addition, IL-1α and β enhanced the cell apoptosis as the same mode as TNF-α. Furthermore, caspase-3 intracellular activity assay (PhiPhiLux^<TM>G_1D_2) showed that the Ltx-induced caspase-3 activation was completely neutralized by CD18 antibody treatment, though the significant neutralization was also observed by CD11a antibody one. Taken together, the present study indicates that TNF-α acts as a potent stimulator of the Ltx-induced HL-60 apoptosis via TNF-receptor 1-mediated upregulation for LEA-1 expression.

Report

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

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Yamaguchi, N., et al.: "TNF-alpha enhances A.actinomycetemcomitans leukotoxin-induced HL-60 cell apoptosis by stimulating LFA-1 expression"Infection and Immunity. 72. 269-276 (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamaguchi, N., et al.: "TNF-alpha enhances A.actinomycetemcomitans leukotoxin-induced HL-60 cell apoptosis by stimulating LFA-1 expression"Infection and Immunity. 72(1). 269-276 (2004)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yamaguchi, N., et al.: "TNF-alpha enhances Actinobacillus actinomycetemcomitans leukotoxin-induced HL-60 cell apoptosis by stimulating LFA-1 expression"Infection and Immunity. 72・1. 269-276 (2004)

    • Related Report
      2003 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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