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In vitro effects of vomitoxin (deoxynivalenol) on T-cell interleukin production and IgA secretion
R L Warner1, K Brooks, J J Pestka
1Department of Food Science & Human Nutrition, Michigan State University, East Lansing 48824.
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.
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.