Murine strain differences in airway inflammation induced by diesel exhaust and house dust mite allergen

2001 Fiscal Year Final Research Report Summary

• Project/Area Number: 12680550
• 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, Departmento of Health Science, Professor, 看護学部, 教授 (50124334)
• Co-Investigator(Kenkyū-buntansha): SUZUKI Akira National Institute for Environmental Studies, Regional Environmental Division, Senior Reseacher of Research Team for Health Effects of Air Pollutants, 大気影響評価研究室, 主任研究員 (20124349)
• Project Period (FY): 2000 – 2001
• Keywords: Diesel exhaust / Bronchial astma / Cytokines / Murin strain difference / Eosinophils / Goblet cells / IgE production / IgGI production

Research Abstract

House dust mites have known to implicate the increase of asthma prevalence today. Three strains of mice (BALB/c, ICR, and C3H/He) were exposed to DE at-a soot concentration of 3.O mg/m^3 or cline air for 8 weeks. These mice injected intratracheally with 1 μ g of Der f four times at 2-week intervals during 8 weeks of the exposure. Histopathological changes in the murine airway, asthma relevant cytokines and chemokines in the lungs, and allergen-specific immunoglobulins in plasma were investigated. DE exposure caused non-ciliated cell proliferation and epithelial cell hypertrophy in the airway of the all strains, and showed very slight goblet cell proliferation in the bronchial epithelium and eosinophil recruitment in the airway of the C3H/He mice. Der f treatment exhibited the recruitment of eosinophils and proliferation of goblet cells in the airway of the three strains. The increasing order of magnitude of those was BALB/c < ICR < C3H/He mice. DE+Der f increased significantly the recruitment of eosinophils in the BALB/c and ICR mice, and increased goblet cell proliferation in the ICR mice compared with Der f treatment. However, these phathologic changes decreased in the case of the C3H/He mice. DE+Der f caused the additional increases of IL-5, eotaxin and RANTES, and synergistic increases of MCP-1 and MIP-1 a in the three strains. The increasing order of IL-5 and eotaxin in lung tissues and Der f-specific lgG1 in plasma by DE+Der f was BALB/c < ICR < C3H/He mice. The production levels of IL-5 in lung tissues corresponded to the manifestations of eosinophilic airway inflammation by DE and/or Der f treatment. The aggravating effect of DE exposure may be mediated mainly by the increase of local expression of IL-5, eotaxin. Antigen-specific lgG1 suggests to be an important immunoglobulin in the pathogenesis of allergic asthma and in the enhancement of DE.