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Modulation of human gp91 ^<phox> gene expression by rickettsia infection

Research Project

Project/Area Number 14570240
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Bacteriology (including Mycology)
Research InstitutionThe Institute of Tropical Medicine, Nagasaki University

Principal Investigator

NAKAMURA Michio  Institute of Tropical Medicine, Nagasaki University, Department of Host-Defense Biochemistry, Professor, 熱帯医学研究所, 教授 (30091276)

Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsEhrlihia / Rickettsia / gp91^<phox> / NADPH oxidase / p47^<phox> / Superoxide / Ehrlichia chaffeensis / 食細胞 / 活性酸素 / HGE / 分化
Research Abstract

To escape from reactive oxygen species generated in response to infection, intracellular pathogens, such as Salmonellae and Anaplasma phagocytophilum, can modulate the expression and distribution of the phagocyte NADPH oxidase components.
In the present study, we analyzed the effect of Ehrlichia chaffeensis infection on the ability of human monocytic THP-1 cells to produce superoxide anion. Phorbol ester-stimulated superoxide generation and mRNA for gp91^<phox> in paralel with mRNAs for p47^<phox>, and p67^<phox> were significantly increased in E. chaffeensis-infected THP-1 cells. These increases were also achieved in THP-1 cells cultured in medium conditioned by the E. chaffeensis-infected cells, indicating that bystander cells can be activated for superoxide generation and implicating soluble factors in the response. Heat-stable and -unstable factors represented one-third and two-thirds of this activity, respectively. These results suggest that immature human monocytic cells increase their ability to generate superoxide anion in response to E. chaffeensis infection regardless they have been directly invaded or not. Further studies have suggested that these factors are exclusively derived from the bacteria.

Report

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

    (4 results)

All 2004 Other

All Journal Article (1 results) Publications (3 results)

  • [Journal Article] Human monocytic cells upregulate superoxide-generating activity and mRNAs for its components in response to heat-stable and heat-unstable factors released to medium conditioned with Ehrlichia chaffeensis-infected THP-1 cells2004

    • Author(s)
      D.Gunasekara, Y.Yoshito, K.Yoshiie, N.Ohashi, M.Nakaniuraa
    • Journal Title

      Acta Medica Nagasakiensia 49

      Pages: 39-44

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Y.Fujii, A.Kumatori, M.Nakamura: "SATB1 makes a complex with p30c and represses gp91^<phox> promoter activity"Microbiol.Immunol.. 47・10. 803-811 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] M.Takata-Yahiro, Y.Fujii, et al.: "A novel GT-mismatch binding protein that recognizes strict DNA sequences with high affinity"Tohoku J.Exp.Med.. 200. 211-229 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 中村三千男: "好中球機能不全"臨床検査. 47・13. 1693-1701 (2003)

    • Related Report
      2003 Annual Research Report

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

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