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Experimental study on pathogenesis of asthma like symptom caused by combination of diesel exhaust and allergen.

Research Project

Project/Area Number 10680528
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 環境影響評価(含放射線生物学)
Research InstitutionOita University of Nursing and Health Sciences

Principal Investigator

ICHINOSE Takamichi  Oita University of Nursing and Health Sciences, Department of Health Sciences, Professor, 看護学部, 教授 (50124334)

Co-Investigator(Kenkyū-buntansha) SUZUKI Akira  National Institute for Environmental Studies, Regional Environmental Division, Senior Researcher of Research Team for Effects of air Pollutants, 大気影響評価研究室, 主任研究員 (20124349)
嵯峨井 勝  国立環境研究所, 大気影響評価研究室, 総括研究官 (80124345)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
KeywordsDiesel exhaust / Bronchial astma / Ovalbumin / Cytokine / Eosinophils / Goblet cells / IgE production / IgG1 produciton / 粘液細胞 / IgG1抗体
Research Abstract

We investigated the histopahologic changes in the airway by long term exposure to diesel exhaust (DE), ovalbumin (OA) treatment or the both combination. The relation between the histopahologic appearances in the airway and immunoglobulin production or levels of local cytokines in the lungs was also studies. ICR mice were exposed to clean air or DE at a soot concentrations of 0.3, 1.0 or 3.0 mg/mィイD13ィエD1 for 34 or 40 weeks. Fifteen weeks after exposures to DE, mice were sensitized intraperitonealy with 10 μg of OA, and challenged aerosol of 1% OA at 3-week intervals during the last 18 or 24 weeks of the exposures. Exposure to DE for 34 weeks caused dose-dependent increases of the typical changes such as non-ciliated cell proliferation and epithelial cell hypertrophy in the airway, but showed no effect on goblet cell proliferation in the bronchial epithelium and eosinophil recruitment in the airway. OA challenge induced very alight changes in goblet cell proliferation and eosinophil rec … More ruitment. The combination of OA and DE exposure at 3.0 mg/mィイD13ィエD1 produced increased changes of goblet cells and eosinophils, in addition to further increases of the typical changes induced by DE. "Exposure to DE at 3.0 mg/mィイD13ィエD1 for 40 weeks also enhanced allergen-induced eosinophil recruitment into the submucos in the airways, and increased protein levels of GM-CSF and IL-5 in the lungs. The increases in the eosinophil recruitment and the local cytokine expression were accompanied by those in goblet cell proliferation in the bronchial epithelium and airway hyperresponsiveness to inhaled acetylcholine. OA treatment induced OA-specific IgG1 and IgE production in plasma, whereas the adjutant effects of DE exposure on the immunoglobulin production were not observed. The present study provides experimental evidence that daily inhalation of DE can enhance the allergen-induced respiratory disease such as allergic asthma. This effect may be mediated mainly by the enhanced local expression of IL-5 and GM-CSF. Less

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Takemichi Ichinose et al: "Long-term exposure todiesel exhaust enhances antigen-induced eossinophilic inflamation and epithelial damage in murin airway"Toxicological Sci. 44. 70-79 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Takamichi Ichinose, Hirohisa Takano, Yuichi Miyabara and Masaru Sagai: "Long-term exposure to diesel exhaust enhances antigen-induced eoshinophilic inflammation and epithelia damage in murine airway"Toxicological Sci. 44. 70-79 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Takamichi Ichinose et al.: "Long-term exposure to diesel exhaust enhances antigen-induced eosinophilic inflammation and epithelial damage in murin airway"Toxicological Sci,. 44. 70-79 (1998)

    • Related Report
      1999 Annual Research Report

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Published: 1998-04-01   Modified: 2025-11-20  

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