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We hypothesized that acute exercise stress would exacerbate immunosuppressive effects of sub-acute exposure to dietary deoxynivalenol (DON). Male BALB/c mice were fed 0 or 2 mg DON/kg diet for 14 days, 12 animals per dose, and then exercised to fatigue on a treadmill. Mice were euthanized by decapitation, trunk blood and spleens were collected. Single-cell suspensions of splenocytes were used to quantify immune function by plaque hemolysis and conconavalin-A (ConA) stimulated lymphocyte proliferation assays. Serum corticosterone level was determined by enzyme immunoassay. Only the nonexercised DON-fed mice showed significant splenocyte proliferation suppression, 32.9 +/- 17.9% of nonexercised controls (p = 0.021). Exercised controls and DON-fed exercised animals showed splenocyte proliferation of 68-75% of nonexercised controls. Antibody response to a T-dependent antigen, sheep red blood cells, was significantly less for exercised DON-fed mice than in controls (p = 0.031). Serum corticosterone levels were significantly higher for both exercised groups compared to the unexercised groups (p < 0.001). IL-4 secretion from mitogen-stimulated splenocytes was elevated by DON alone (p < 0.05) while IL-2 was elevated by DON with exercise stress (p < 0.05). Our hypothesis was confirmed with respect to T-lymphocyte-dependent antibody production, but not for splenocyte proliferation. Exercise stress abrogated DON-mediated suppression of splenocyte proliferation, perhaps mediated by induction of elevated stress hormones counteracting cytokine expression alterations of DON.

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