In vitro effects of vomitoxin (deoxynivalenol) on T-cell interleukin production and IgA secretion.

The exposure of lymphocyte cultures to vomitoxin was used to determine possible mechanisms by which this naturally occurring toxin induces serum immunoglobulin A (IgA) elevation and IgA nephropathy in the mouse. Vomitoxin exposure within the range of 10 to 1000 ng/ml inhibited DNA synthesis, protein synthesis as well as IgA, IgG and IgM production in lymphocyte cultures prepared from the Peyer's patch (PP) and spleen. When purified B cells were cultured in the presence of vomitoxin, inhibition of IgA, IgG and IgM production was similarly observed. However, on 24-hr pulsed co-exposure to vomitoxin and the mitogen concanavalin A (ConA), CD4+/CD8+ cells were capable of inducing a three- to five-fold increase in production of IgA, but not IgG and IgM by cocultured B cells when compared with B cells cocultured with control T cells exposed to the mitogen only. When pulsed for 48 hr with ConA and toxin, CD4+ cells were similarly capable of causing a significant increase in IgA production by B cells. 48-hr pulsed exposure of CD4+ cells to ConA and vomitoxin resulted in significantly increased production of the T helper cytokines IL-4, IL-5 and IL-6 after 5 additional days of culture, compared with ConA-stimulated CD4+ cells alone. These results suggest that vomitoxin was capable of enhancing CD4(+)-mediated help for IgA production by B cells and that this could possibly be mediated by way of increased cytokine production.