Summary: | 碩士 === 國立中興大學 === 獸醫學系暨研究所 === 107 === Atopic dermatitis(AD) is a multifactorial disease process. It is defined as a genetically predisposed biphasic inflammatory and pruritic allergic skin disease often associated with a production of immunoglobulin E (IgE) against environmental allergens. A predominant systemic Th2 disbalance with increased IgE levels and eosinophilia is widely accepted in the pathogenesis of atopic diseases. The production of Th2 mediated cytokines, notably IL-4, IL-5, and IL-13, can be detected in skin during the acute phase of disease. FIPs (Fungal immunomodulatory proteins) had the ability to induct cytokine expression. GMI (G. microsporum immunomodulatory protein), a FIP cloned from G. microsporum, contains 111 amino acids, with the amino acid sequence highly homologous with those of the other FIPs, including LZ-8. Evidence indicates that purified and recombinant GMI displays remarkable anti-inflammatory and anti-tumor effects. In this study, we assessed the anti-inflammatory and anti-allergic effects of GMI on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in rats. Thirty male 7-weeks-old Sprague-Dawley rats were randomly divided into 6 groups. The rats received DNCB topically application on the back for two weeks to induce AD-like lesions, and then treated with GMI and prednisolone for four weeks. Our results demonstrated that the number of inflammatory cells were decreased after exposure of GMI (P <0.01), and the expression level of immunoglobulin E, dermatitis scores, epidermal thickness and mast cells were all reduced in a dose dependent manner (P <0.01). Additionally, our results showed that the GMI had similar efficacy to prednisolone. Based on this evidence, we believe that GMI could ameliorate the DNCB-induced atopic dermatitis in rats. It also possesses the potential to be used as an adjuvant therapy for allergic diseases. However, the mechanisms of the modulation on T cells and the safety of GMI need further studies for use as an ideal treatment strategy.
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