Experimental study on pathogenesis of asthma like symptom caused by combination of diesel exhaust and allergen.
Project/Area Number |
10680528
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
環境影響評価(含放射線生物学)
|
Research Institution | Oita 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)
|
Keywords | Diesel 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)
Research Products
(3 results)