PetCaseFinder

Peer-reviewed veterinary case report

Induction of allergic dermatitis with dinitrofluorobenzene in Yama mice.

Journal:
Methods in cell biology
Year:
2026
Authors:
Yamada-Satchwell, Yusuke et al.
Affiliation:
Joint Faculty of Veterinary Medicine · Japan
Species:
rodent

Abstract

Allergic dermatitis (AD) is a skin disease characterized by chronic inflammation. In the early stage, swollen, rush, hyperemia, and so on, are observed and moreover thickening and lichenification of the skin can occur at chronic stage. Most case of ADs are type Ⅰ allergy and immunoglobulin E and chemical such as histamine are involved. Type Ⅰ allergy is considered to be Th2 immunoreaction. Furthermore, lesions of AD contain eosinophil that play a role in Th2 immunoreaction. Clinically, lichenification lesions are refractory and dermal fibrosis and epidermal thickening are visible histopathologically. Mast cells and eosinophils are considered to be involved in dermal fibrosis in AD however the mechanism is not uncovered. There are two accessible preexisting models of AD, chemically induced models using BALB/c mice and naturally occurring model of NC/Nga mice, although their fibrosis of derms weak unfortunately that make them unsuitable for analyzing refractory AD. Yama mouse, novel inbred mouse strain, demonstrates eosinophilia with elevated eosinophil in peripheral blood and bone marrow. Naive Yama mouse has no organ failure and pathological change. When the mouse induced AD chemically, the lesions contain severe infiltration of eosinophil and severe dermal fibrosis. This novel mouse model can develop research area of AD. Here, we aim to describe the detailed procedure of developing AD mouse model with two preexisting and the novel mouse models with focusing of the difference in three models.

Find similar cases for your pet

PetCaseFinder finds other peer-reviewed reports of pets with the same symptoms, plus a plain-English summary of what was tried across them.

Search related cases →

Original publication: https://pubmed.ncbi.nlm.nih.gov/41724568/