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Updated: Jul 13, 2026

Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Epicutaneous sensitization in BALB/c mice induces stronger systemic Th2 inflammation than intranasal sensitization
Hiromi Nagano1, Takayuki Kyutoku1, Hayato Matsumoto1
1Department of Otolaryngology Head and Neck Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Abstract:
<b>Introduction:</b> Epicutaneous sensitization (ES) plays a role in the onset of allergic diseases such as atopic dermatitis (AD), bronchial asthma, and food allergies, but its effects on nasal allergic diseases remain unclear. <br><br><b>Aim:</b> The aim of this study was to compare the effects of intranasal challenge following ES with those following intranasal sensitization (NS) on nasal allergic inflammation. <br><br><b>Materials and methods:</b> Female BALB/c mice were sensitized epicutaneously or intranasally with 25 μg of ovalbumin (OVA) and 2 μg of cholera toxin (CT) six times at weekly intervals. These groups were compared with control groups that received ES with phosphate- buffered saline (PBS) alone, OVA alone, or CT alone. Two weeks after the final sensitization, the mice were challenged intranasally with 500 μg of OVA ten times over a two-week period. Four weeks after the final sensitization, allergic inflammation in the nasal cavity, OVA-specific IgE production, and cytokine profiles were evaluated in the different groups. <br><br><b>Results:</b> Post-challenge, there was no significant difference in the number of eosinophils or the thickness of lateral nasal mucosa between the ES and NS groups. However, the serum level of OVA-specific IgE in the ES group was significantly higher than that in the control and NS groups. Levels of IL-4, IL-5, IL-13, and IL-33 in CD4+ T cells were also significantly higher in the ES group than in the NS group. <br><br><b>Conclusions:</b> These results indicate that intranasal challenge following ES induces comparable eosinophilic inflammation in the nasal cavity, but elicits a stronger systemic Th2-type inflammatory response than that following NS.
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