Establishment and Characterization of Mild Atopic Dermatitis in the DNCB-Induced Mouse Model

Author:

Riedl Rebecca12,Kühn Annika2ORCID,Rietz Denise1,Hebecker Betty23,Glowalla Karl-Gunther4,Peltner Lukas K.5ORCID,Jordan Paul M.56ORCID,Werz Oliver56ORCID,Lorkowski Stefan23ORCID,Wiegand Cornelia1,Wallert Maria23ORCID

Affiliation:

1. Department of Dermatology, University Hospital Jena, Dermatological Research Laboratory, 07747 Jena, Germany

2. Department of Nutritional Biochemistry and Physiology, Institute of Nutritional Science, Friedrich Schiller University, 07743 Jena, Germany

3. Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, 07743 Jena, Germany

4. Service Unit Experimental Biomedicine, Friedrich Schiller University, 07745 Jena, Germany

5. Department of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich Schiller University, 07743 Jena, Germany

6. Jena Center for Soft Matter (JCSM), Friedrich Schiller University, 07743 Jena, Germany

Abstract

In dermatological research, 2,4-dinitrochlorbenzene (DNCB)-induced atopic dermatitis (AD) is a standard model as it displays many disease-associated characteristics of human AD. However, the reproducibility of the model is challenging due to the lack of information regarding the methodology and the description of the phenotype and endotype of the mimicked disease. In this study, a DNCB-induced mouse model was established with a detailed procedure description and classification of the AD human-like skin type. The disease was induced with 1% DNCB in the sensitization phase and repeated applications of 0.3% and 0.5% DNCB in the challenging phase which led to a mild phenotype of AD eczema. Pathophysiological changes of the dorsal skin were measured: thickening of the epidermis and dermis, altered skin barrier proteins, increased TH1 and TH2 cytokine expression, a shift in polyunsaturated fatty acids, increased pro-resolving and inflammatory mediator formation, and dysregulated inflammation-associated gene expression. A link to type I allergy reactions was evaluated by increased mast cell infiltration into the skin accompanied by elevated IgE and histamine levels in plasma. As expected for mild AD, no systemic inflammation was observed. In conclusion, this experimental setup demonstrates many features of a mild human-like extrinsic AD in murine skin.

Funder

Free State of Thuringia and the European Social Fund

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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