ovalbumin and nivalenol

Nivalenol (NIV) has been reported to induce hyperproduction of IgA, which is regulated by T-helper 2 cells (Th2); however, whether IgE production, which is under the regulation of Th2 cells, is induced by this compound remains largely unknown. We examined the effect of NIV on antigen-specific IgE production using ovalbumin (OVA)-specific T cell receptor alphabeta-transgenic mice. The mice produced significant amounts of total and antigen-specific IgE, IgG1, and IgA in serum when given OVA orally. Administration of NIV with OVA suppressed total IgE and OVA-specific IgE, IgG1, and IgA production significantly. Cytokine assay using splenocytes obtained from mice given the OVA plus NIV diet revealed that interleukin 4 (IL-4) production was suppressed and interleuin-2 (IL-2) production was enhanced. These results suggest that the inhibition of IL-4 production and enhancement of IL-2 production induced by NIV suppressed total and antigen-specific IgE production.

Topics: Animals; Antibody Formation; Immunoglobulin E; Interleukin-2; Interleukin-4; Male; Mice; Mice, Inbred BALB C; Mice, Transgenic; Mycotoxins; Ovalbumin; Th2 Cells; Trichothecenes