Quantitative Analysis of Histopathological Changes in an Animal Model of Dinitrochlorobenzene-Induced Atopic Dermatitis: Correlation with Serum Total IgE Levels

Document Type : Original Articles

Authors

1 Department of Internal Medicine, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran

2 Department of Parasitology, Faculty of veterinary medicine, University of Tehran, Tehran, Iran

3 Department of Pathology, Faculty of veterinary medicine, University of Tehran, Tehran, Iran

4 Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran

10.22059/ijvm.2025.386903.1005707

Abstract

Background: The mouse model of atopic dermatitis plays a vital role in the development of new therapies, facilitating the assessment of drug impacts and the investigation of disease mechanisms. Its genetic and physiological traits closely resemble those of mammals, making it an effective system for replicating symptoms and studying the molecular processes associated with inflammation and immune responses.
Objective: The aim of this study was to evaluate the histopathological characteristics and identify quantitative metrics of the epidermis and dermis, as well as serum IgE levels, in a mouse model of atopic dermatitis induced by dinitrochlorobenzene (DNCB) in order to guide future studies trying to develope novel therapies for atopy.
Methods: A total of 12 mice were divided into two groups: one group was induced with atopic dermatitis using dinitrochlorobenzene (DNCB), while the control group received a vehicle. Microscopic analysis of skin samples assessed dermal and epidermal thickness and eosinophilic infiltration using hematoxylin and eosin staining. Mast cell counts were determined with toluidine blue staining, and serum levels of total IgE were measured using a murine-specific ELISA kit.
Results: The evaluation of skin and serum samples indicated that dermal and epidermal thickness, as well as eosinophil and mast cell infiltration, and serum IgE levels were significantly elevated in the DNCB-induced group.
Conclusion: This study demonstrates that the DNCB-induced mouse model of atopic dermatitis effectively replicates key histopathological features, including increased dermal and epidermal thickness, eosinophil and mast cell infiltration, and elevated serum IgE levels. These findings enhance our understanding of the disease and support future therapeutic development. Our results can help researchers determine quantitative parameters measuring the efficacy of novel drugs proposed for alleviating atopic signs.

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