Atopic dermatitis is a chronic or recurrent pruritic inflammatory skin disease. The association of such skin lesions with infiltration by T cells, eosinophils, mast cells and other cells suggests underlying complex immune dysfunction. Repeated exposure of the skin to house dust mite allergen Der f and staphylococcal enterotoxin SEB induces AD-like skin lesions, accompanied by elevated serum IgE levels in mice. House dust mite-derived serine proteases activate PAR‑2 on keratinocytes, thereby inducing the production of ET‑1 and matrix metalloproteinase‑9 (MMP‑9), which contribute to the generation of pruritus in atopic dermatitis. ET‑1 is a polypeptide synthesized by various cell types, including endothelial cells, vascular smooth muscle cells, keratinocytes and inflammatory cells. ET‑1‑mediated pruritus involves both direct action on pruritic nerve endings and indirect effects via the release of endogenous mediators such as histamine. Intradermal injection of ET‑1 mainly elicits scratching responses by activating endothelin‑A receptors on mast cells and sensory neurons. SEB can trigger inflammatory responses in the skin, thereby exacerbating and sustaining cutaneous inflammation in mice.

C57BL/6 mice (male and female, about 6–8 weeks old)

Modeling method: Cosmetic cotton pads loaded with Der f and SEB were fixed on the depilated dorsal region. After several days, the pads were removed and the mice were allowed to rest for a period. After 3 repeated rounds, the atopic dermatitis model was successfully established.

Positive drug: Not specified

Evaluation indicators: clinical appearance score, ELISA assay, HE staining, toluidine blue staining

Clinical appearance score

ELISA assay

HE staining of skin tissue

Toluidine blue staining of skin tissue