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Peer-reviewed veterinary case report

Epicutaneous sensitization in BALB/c mice induces stronger systemic Th2 inflammation than intranasal sensitization despite comparable nasal eosinophilia.

Journal:
Otolaryngologia polska = The Polish otolaryngology
Year:
2026
Authors:
Nagano, Hiromi et al.
Affiliation:
Department of Otolaryngology Head and Neck Surgery · Japan
Species:
rodent

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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Original publication: https://pubmed.ncbi.nlm.nih.gov/41717816/