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Updated: Sep 27, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Differences in airway-inflammation development by house dust mite and diesel exhaust inhalation among mouse strains
Takamichi Ichinose1, Hirohisa Takano, Kaori Sadakane
1Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Notsuharu, Oita 870-1201, Japan.
Abstract:
Three mouse strains (BALB/c, ICR, and C3H/He) were injected intratracheally with house dust mites (Der f) four times at 2-week intervals during exposure to diesel exhaust (DE) or clean air for 8 weeks. Der f treatment caused eosinophilic inflammation and proliferation of goblet cells in the airways of the three strains. DE + Der f caused a further increase of eosinophils in BALB/c and ICR mice, but not in C3H/He mice. DE + Der f significantly increased interleukin (IL)-5; regulated on activation, normal T cell expressed, and presumably secreted (RANTES); eotaxin, monocyte chemotactic protein-1 (MCP-1); and macrophage-inflammatory protein-1 alpha (MIP-1 alpha) in all three strains. However, the protein of IL-5 decreased more in C3H/He mice treated with DE + Der f than in mice treated with Air + Der f. The levels of IL-5 in lung tissues corresponded to the pathological changes by Der f and/or DE treatment. The levels of MCP-1 and MIP-1 alpha in the three strains corresponded to the accumulation of lymphocytes in the airway. The adjuvant effect of DE on IgG1 production was observed in the ICR and C3H/He mice. These results suggest that the murine strain differences in the production of eosinophilic airway inflammation by DE + Der f is related to differences in local expression of IL-5, eotaxin, and IgG1 production. The enhancing effects of DE exposure may be mediated mainly by local IL-5.
Insights
Diesel exhaust (DE) exposure exacerbates house dust mite (Der f)-induced airway inflammation, with strain-dependent differences in eosinophil and cytokine responses. These effects are linked to local interleukin-5 (IL-5) expression.
Area of Science:
- Immunology
- Environmental Health
- Respiratory Medicine
Background:
- House dust mites (Der f) are common allergens that trigger airway inflammation.
- Diesel exhaust (DE) is a major air pollutant with known respiratory effects.
- Understanding the combined impact of allergens and pollutants is crucial for public health.
Purpose of the Study:
- To investigate the synergistic effects of diesel exhaust (DE) and house dust mite (Der f) exposure on airway inflammation in different mouse strains.
- To identify strain-specific differences in inflammatory responses and cytokine profiles.
- To elucidate the role of local cytokine expression in mediating these effects.
Main Methods:
- Three mouse strains (BALB/c, ICR, C3H/He) were exposed to DE or clean air.
- Mice received intratracheal injections of Der f.
- Airway inflammation, goblet cell proliferation, and levels of cytokines (IL-5, RANTES, eotaxin, MCP-1, MIP-1 alpha) and IgG1 were assessed.
Main Results:
- Der f induced eosinophilic inflammation and goblet cell hyperplasia in all strains.
- DE + Der f increased eosinophils in BALB/c and ICR mice, but not C3H/He.
- DE + Der f significantly elevated multiple pro-inflammatory cytokines (IL-5, RANTES, eotaxin, MCP-1, MIP-1 alpha) across strains.
- DE enhanced IgG1 production in ICR and C3H/He mice.
- Local IL-5 levels correlated with inflammation severity and strain differences.
Conclusions:
- Murine strain differences in response to DE + Der f are associated with variations in local IL-5, eotaxin, and IgG1 production.
- DE exposure potentiates Der f-induced airway inflammation, primarily mediated by local IL-5.
- These findings highlight the complex interplay between environmental pollutants and allergens in respiratory diseases.
