Topical application of Taglisodog-eum inhibits the development of experimental atopic dermatitis

AIM OF STUDY: Taglisodog-eum (, Tuo Li Xiao Du Yin), a standardized herbal formula, has been widely used to modulate diverse carbuncles in oriental medicine. However, it is still unclear whether Taglisodog-eum (TSE) can exert a beneficial role in dermatological disease. In this study, we examined the effect of topical application of TSE on experimental atopic dermatitis (AD) and elucidated its action mechanism. MATERIALS AND METHODS: To test the effect of TSE treatment on IgE production in vitro, U266B1 cells and primary CD19⁺ B cells isolated from AD-induced mice were treated with TSE under LPS/IL-4 stimulation and then IgE level in the culture supernatant was measured by ELISA. To evaluate the effect of TSE treatment on the production of AD related pathogenic cytokines, CD4⁺ T cells isolated from AD-induced mice were treated with TSE under PMA/ionomycin stimulation, then the level of cytokine expression was analyzed by quantitative RT-PCR and ELISA. The effects of TSE on the NFκB promoter activity in T cells and on the expression level of Aicda (activation-induced cytidine deaminase) in B cells were examined. To further examine the in vivo efficacy of TSE on AD progression, TSE was topically applied to ears of mice with atopic dermatitis induced by painting of DNCB and house dust mite extract. AD Progression was estimated by following criteria: (a) ear thickness, clinical score, (b) serum total IgE and mite specific IgE level by ELISA, (c) histological examination of ear tissue by H&E staining and (d) cytokine profile of total ear cells and draining lymph node CD4⁺ T cells by quantitative real time PCR and ELISA. RESULTS: Treatment of TSE to the U266B1 cell line and primary CD19⁺ B cells isolated from AD-induced mice inhibited IgE production. Treatment of TSE down-regulated the expression of several cytokines (IL-4, IL-10, IL-13, IL-17, TNF-α and IFN-γ) in CD4⁺ T cells isolated from AD-induced mice. Topical application of TSE on the ears of AD-induced mice decreased the severity and progression of disease by reducing ear thickness, clinical scores including dryness, edema. TSE treatment reduced the infiltration of lymphocytes to the inflamed site analyzed by histological evaluation. TSE treatment also decreased serum IgE level and expression of AD-associated pathogenic cytokines (IL-4, IL-5 and IL-13) in total ear cells and dLN CD4⁺ T cells by inhibiting the translocation of NFκB into nucleus. CONCLUSIONS: Our study indicates that protective effect of Ta