Combined application of dinitrofluorobenzene and ovalbumin induced AD-like dermatitis with an increase in helper T-cell cytokines and a prolonged Th2 response

Background: The progression of acute-to-chronic atopic dermatitis is accompanied by multiple helper T-cell cytokine responses, but the mechanisms and relative importance of these changes remain unclear. There is no animal model for atopic dermatitis that recapitulates these cytokine responses.

Objective: We sought to build a novel mouse model for atopic dermatitis (AD) that recapitulates these helper T-cell responses and some dynamic changes in cytokine responses in the progression of AD.

Methods: Female BALB/c mice were subjected to the application of dinitrofluorobenzene (DNFB) and ovalbumin (OVA) to induce AD-like dermatitis. Skin lesions and serum were collected from mice in the acute and chronic phases to detect changes in cytokine responses and other features of AD.

Results: Combined application of DNFB and OVA successfully induced AD-like dermatitis and histological changes as well as epidermal barrier dysfunction. In the acute phase of AD-like dermatitis, Th2-associated cytokines were mainly increased in serum and skin lesions. In the chronic phase of AD-like dermatitis, Th2-associated cytokines were still highly expressed, while Th1- and Th17-associated cytokines were also gradually increased. Compared with the acute phase, the JAK-STAT signaling pathway was highly expressed in the chronic phase of AD-like dermatitis.

Conclusion: The combined application of DNFB and OVA could be used to build a new mouse model for atopic dermatitis. This mouse model recapitulates the helper T-cell responses and some dynamic changes in cytokine responses in the progression of acute-to-chronic in human AD. The JAK-STAT signaling pathway plays a pivotal role in the chronicity of AD.