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.
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.
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.
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.
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.