Nakamura Tomoya, Yoshida Naoki, Nishibu Akiko, Mochizuki Takashi
Department of R&D Center, Ikeda Mohando Co., Ltd.
Department of Dermatology, Kanazawa Medical University.
Med Mycol J. 2019;60(3):65-70. doi: 10.3314/mmj.19.005.
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 β-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.
须发癣菌引起的浅表皮肤真菌病在人类患者中的患病率非常高。皮肤癣菌通常感染表皮，尤其是角质层，形成鳞屑、角化过度和水疱。免疫系统在须发癣菌感染中发挥的重要作用是检测真菌入侵和清除真菌。这些免疫机制被认为不仅涉及固有免疫，还涉及获得性免疫。因此，迫切需要基于新的基础知识开展治疗方法的研究，阐明须发癣菌诱导的炎症反应的免疫机制尤为重要。然而，由于须发癣菌无法在小鼠皮肤上定殖，我们尝试使用基于接触性超敏反应的方法，开发一种由从须癣毛癣菌中提取的癣菌素诱导的须发癣菌炎症模型。癣菌素是一种粗提物，主要含有包括β-葡聚糖和酵母聚糖在内的真菌细胞壁成分。在该模型中，TLR2、TLR4和dectin-1高表达，并观察到IL-17A和IL23的产生。这表明我们成功地在小鼠中诱导了真菌特异性炎症。在这篇综述中，我们介绍了一种为研究须发癣菌诱导的炎症反应的免疫机制而开发的小鼠须发癣菌炎症模型。此外，我们报告了使用该炎症模型评估抗真菌药物的抗炎和止痒效果的结果。
