A Mouse Model of Trichophyton Inflammation Based on Trichophytin-induced Contact Hypersensitivity

The prevalence of Trichophyton-induced superficial skin mycosis is very high among human patients. Dermatophytes generally infect the epidermis, especially the stratum corneum, forming scales, hyperkeratosis, and vesicles. The important roles played by the immune system in Trichophyton infection are detection of fungal invasion and elimination of fungi. These immune mechanisms are presumed to involve not only innate immunity but also acquired immunity. Therefore, there is a substantial need for studies on treatment methods based on new basic knowledge, and the elucidation of immunological mechanisms of Trichophyton-induced inflammatory reactions is especially important. However, since Trichophyton cannot colonize on the mouse skin, we tried to develop a model for Trichophyton inflammation induced by trichophytin extracted from Trichophyton mentagrophytes using a method based on contact hypersensitivity. Trichophytin is a crude extract that mainly contains fungal cell wall constituents including beta-glucan and zymosan. In this model, TLR2, TLR4, and dectin-1 were highly expressed, and production of IL-17A and IL23 was observed. This indicates that we succeeded in inducing fungal-specific inflammation in the mice. In this review, we introduce a mouse Trichophyton inflammation model developed to investigate the immunological mechanisms of Trichophyton-induced inflammatory reactions. In addition, we report results of evaluation of anti-inflammatory and anti-itching effects of anti-fungal agents using the inflammation model.