Abstract
Fumonisins are one of the fungal toxins produced by Fusarium species. Fumonisin B3 (FB3), a member of the fumonisin B group, is known to inhibit the biosynthesis of sphingolipids by inhibiting ceramide synthesis, but the toxic effects caused by FB3 remain unclear. We herein investigated the effects of FB3 on allergy using an atopic dermatitis (AD) mouse model. The AD model was generated by topical application of 2,4-tolylene diisocyanate (TDI) in female NC/Nga mice. FB3 (0.1%) was administered topically before each TDI application. AD score and trans epidermal water loss (TEWL) were measured weekly. One day after the last TDI application, auricular lymph nodes (LN), serum and skin samples were collected for analysis of the number of immunocompetent cells, cytokine level, total IgE level, and related gene expression. FB3 treatment significantly increased AD score compared to the AD control group. The numbers of helper T cells and IgE-producing B cells in LN were significantly increased by FB3 treatment, whereas there were no significant differences in cytokine production and serum IgE level. The gene expression of IL-33, which is involved in the exacerbation of AD, was significantly increased in the FB3 group. Significant upregulation of TEWL in FB3 group reveals that FB3 breakdowns the cutaneous barrier function, corroborated by a significant influence of the related genes expression (Cers3 and Degs1) in FB3 group. Our findings suggest that FB3 exacerbates AD by breakdown the cutaneous barrier function and activating IL-33 expression.
