Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis.

2,4-dinitrochlorobenzene atopic dermatitis mouse model mild and moderate atopic dermatitis sub-acute and chronic inflammation

Journal

Inflammation
ISSN: 1573-2576
Titre abrégé: Inflammation
Pays: United States
ID NLM: 7600105

Informations de publication

Date de publication:
27 Dec 2023
Historique:
received: 10 11 2023
accepted: 04 12 2023
revised: 10 11 2023
medline: 27 12 2023
pubmed: 27 12 2023
entrez: 27 12 2023
Statut: aheadofprint

Résumé

The mouse model of 2,4-dinitrochlorbenzene (DNCB)-induced human-like atopic dermatitis (hlAD) has been widely used to test novel treatment strategies and compounds. However, the study designs and methods are highly diverse, presenting different hlAD disease patterns that occur after sensitization and repeated challenge with DNCB on dorsal skin. In addition, there is a lack of information about the progression of the disease during the experiment and the achieved pheno- and endotypes, especially at the timepoint when therapeutic treatment is initiated. We here examine hlAD in a DNCB-induced BALB/cJRj model at different timepoints: (i) before starting treatment with dexamethasone, representing a standard drug control (day 12) and (ii) at the end of the experiment (day 22). Both timepoints display typical AD-associated characteristics: skin thickening, spongiosis, hyper- and parakeratosis, altered cytokine and gene expression, increased lipid mediator formation, barrier protein and antimicrobial peptide abnormalities, as well as lymphoid organ hypertrophy. Increased mast cell infiltration into the skin and elevated immunoglobulin E plasma concentrations indicate a type I allergy response. The DNCB-treated skin showed an extrinsic moderate sub-acute hlAD lesion at day 12 and an extrinsic mild sub-acute to chronic pheno- and endotype at day 22 with a dominating Th2 response. A dependency of the filaggrin formation and expression in correlation to the disease severity in the DNCB-treated skin was found. In conclusion, our study reveals a detailed classification of a hlAD at two timepoints with different inflammatory skin conditions and pheno- and endotypes, thereby providing a better understanding of the DNCB-induced hlAD model in BALB/cJRj mice.

Identifiants

pubmed: 38150167
doi: 10.1007/s10753-023-01943-x
pii: 10.1007/s10753-023-01943-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Free State of Thuringia and the European Social Fund
ID : 2019 FGR 0095
Organisme : Free State of Thuringia and the European Social Fund
ID : 2019 FGR 0095
Organisme : Free State of Thuringia and the European Social Fund
ID : 2019 FGR 0095
Organisme : Free State of Thuringia and the European Social Fund
ID : 2019 FGR 0095

Informations de copyright

© 2023. The Author(s).

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Auteurs

Rebecca Riedl (R)

Department of Dermatology, Dermatological Research Laboratory, Jena University Hospital, 07747, Jena, Germany.
Department of Biochemistry and Physiology of Nutrition, Institute of Nutritional Science, Friedrich Schiller University, 07743, Jena, Germany.

Annika Kühn (A)

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

Yvonne Hupfer (Y)

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

Betty Hebecker (B)

Department of Biochemistry and Physiology of Nutrition, Institute of Nutritional Science, Friedrich Schiller University, 07743, Jena, Germany.
Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, 07743, Jena, Germany.

Lukas K Peltner (LK)

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

Paul M Jordan (PM)

Department of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich Schiller University, 07743, Jena, Germany.
Jena Center for Soft Matter (JCSM), Friedrich Schiller University, 07743, Jena, Germany.

Oliver Werz (O)

Department of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich Schiller University, 07743, Jena, Germany.
Jena Center for Soft Matter (JCSM), Friedrich Schiller University, 07743, Jena, Germany.

Stefan Lorkowski (S)

Department of Biochemistry and Physiology of Nutrition, Institute of Nutritional Science, Friedrich Schiller University, 07743, Jena, Germany.
Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, 07743, Jena, Germany.

Cornelia Wiegand (C)

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

Maria Wallert (M)

Department of Biochemistry and Physiology of Nutrition, Institute of Nutritional Science, Friedrich Schiller University, 07743, Jena, Germany. maria.wallert@uni-jena.de.
Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, 07743, Jena, Germany. maria.wallert@uni-jena.de.

Classifications MeSH