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Crosstalk between transcription factors responsive to LPS and anti-inflammatory agents

Research Project

Project/Area Number 13671957
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Functional basic dentistry
Research InstitutionOsaka Dental University

Principal Investigator

OHURA Kiyoshi  Osaka Dental University, Dentistry, Professor, 歯学部, 教授 (20131378)

Co-Investigator(Kenkyū-buntansha) AZUMA Yasutaka  Osaka Dental University, Dentistry, Assistant, 歯学部, 助手 (50298816)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
KeywordsPPARγ / macrophages / natural immunity / inflammation / nuclear transcription factor / prostaglandins
Research Abstract

15-Deoxy-Δ^<12,14>-prostaglandin J_2 (dPGJ_2) is a metabolite of prostaglandin D_2, that binds to peroxisome proliferator-activated receptor γ (PPARγ). PPARγ and prostaglandin D_2 synthase, which is required for dPGJ_2 synthesis, are predominantly expressed in macrophages. In contrast, IL-10 and IL-12 produced by macrophages stimulate Th1 and Th2 immune response, respectively. This study investigated the effect of dPGJ_2 on IL-10 and IL-12 production by macrophages in response to lipopolysaccharide (LPS). Our data clearly demonstrated that dPGJ_2 inhibits LPS-induced IL-10 and IL-12 production by macrophages. A different agonist of PPARγ, *3-hydroxyoctadecadienoic acid, similarly inhibited the production of IL-10 and IL-12 in response to LPS. Further, dPGJ_2 did not appear to act through the PGD_2 receptor. These results suggest that dPGJ_2 may inhibit LPS-induced IL-10 and IL-12 production by macrophages through PPARγ. Prostaglandin D_2 (PGD_2) acts via the adenyl cyclase-coupled receptor for PGD_2 (DP receptor). Here we present evidence that BW245C, a DP receptor agonist, modulates macrophage functions related to natural immunity. BW245C inhibited macrophage chemotaxis at concentrations of 0.1 to 10 μM and phagocytosis of Escherichia coli by macrophages at a concentration of 10 μM. In addition, BW245C inhibited the production of superoxide anion by PMA-stimulated macrophages at concentrations of 0.1 to 10 μM and nitrite production by LPS-stimulated macrophages at a concentration of 10 μM. In contrast, BW245C potentiated the production of TNF-α, a pro-inflammatory cytokine, by LPS-stimulated macrophages at concentrations of 1 to 10 μM. These results suggest that PGD_2 may modulate macrophage functions related to natural immunity via DP receptor.

Report

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

    (11 results)

All Other

All Publications (11 results)

  • [Publications] Yasutaka Azuma: "15-Deoxy-Δ^<12,14>-prostaglandin J_2 is a negative regulator of macrophage functions"International Immunopharmacology. 1. 2101-2108 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kiyoshi Daito: "Simultaneous determination of alteration of a variety of macrophage functions related to natural immunity following treatment with DP receptor agonist"Japanese Journal of Oral Biology. 44. 522-529 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Azuma Y, Shinohara M, Wang P-L and Ohura K: "15-Deoxy-Δ^<12,14>-prostaglandin J_2 a negative regulator of macrophage functions"International Immunopharmacology. 1(12). 2101-2108 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Azuma Y, Shinohara M and Ohura K: "Inhibition of macrophage functions by signaling of PPARγ"Folia Pharmacologica Japonica. 118(4). 28 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Daito K, Azuma Y, Daito M and Ohura K: "Simultaneous determination of alteration of a variety of macrophage functions related to natural immunity following treatment with DP receptor agonist"Japanese Journal of Oral Biology. 44(6). 522-529 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Azuma Y and Ohura K: "Alteration of macrophage functions by signaling of 15-Deoxy-Δ^<12,14>-prostaglandin J_2"Oral Therapeutics and Pharmacology. 21(3). 119 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Watanabe K, Azuma Y, Daito M, Shinohara M and Ohura K: "Possible interaction of thiazolidine derivatives curative agent for diabetes with immune functions of macrophages related to natural immunity"Abstracts of 2th Research Summary of High-Technology Research Project in Osaka Dental University. 14 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Daito K, Azuma Y, Daito M and Ohura K: "Alteration of macrophage functions by signaling of prostaglandin D_2"Japanese Journal of Oral Biology. 44(5). 474 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Yasutaka Azuma: "15-Deoxy-Δ^<12,14>-prostaglandin J_2 is a negative regulator of macrophage functions"International Immunopharmacology. 1(12). 2101-2108 (2001)

    • Related Report
      2002 Annual Research Report
  • [Publications] Kiyoshi Daito: "Simultaneous determination of alteration of a variety of macrophage functions related to natural immunity following treatment with DP receptor agonist"Japanese Journal of Oral Biology. 44(6). 522-529 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Yasutaka Azuma: "15-Deoxy-Δ^<12,14>-prostaglandin J_2 is a negative regulator of macrophage functions"International Junnunopharniacology. 1(12). 2101-2108 (2001)

    • Related Report
      2001 Annual Research Report

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

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