Ochratoxin A (OA) was incorporated in the diets of growing gilts (mean body weight, 20.1 kg) at a concentration of 2.5 mg of OA/kg of feed and was fed continuously for 35 days. Humoral and cell-mediated immunologic measurements were evaluated to determine the effects of OA on immune function in swine. Cutaneous basophil hypersensitivity to phytohemagglutinin (PHA), delayed hypersensitivity to tuberculin, PHA-induced lymphocyte blastogenesis, interleukin-2 production, total and isotype immunoglobulin concentrations, antibody response to chicken RBC, and macrophage activation were used to evaluate immune function. Gilts treated with OA had reduced cutaneous basophil hypersensitivity response to PHA reduced delayed hypersensitivity to tuberculin, decreased stimulation index for lymphoblastogenesis, decreased interleukin-2 production when lymphocytes were stimulated with concanavalin A, and decreased number and phagocytic activity of macrophages. Differences were not observed for total and isotype immunoglobulin concentrations, or humoral hemagglutination (chicken RBC) titer. These data indicate that OA may suppress cell-mediated immune response in growing swine.

Porcine blood mononuclear cells (BMC) were exposed to prepartum concentration of estrogen in gilts before acquisition (in vivo), and their subsequent reactivity (in vitro) was explored. In a cross-over experimental designed study, 6 ovariectomized gilts were injected once with 3.75 mg of estradiol-17beta benzoate in arachidic oil or with arachidic oil only during 2 experiments. The ability of their BMC to proliferate in response to stimulation with phytohemagglutinin, concanavalin A, and pokeweed mitogen was assayed in cultures of blood and in cultures of purified BMC. After 2 days of mitogen stimulation, activity of accessible interleukin 2 was quantified in supernatants obtained from cultures of purified BMC and supernatants of blood cultures stimulated with pokeweed mitogen. Also, production of immunoglobulins by purified BMC in response to polyclonal stimuli was measured. Three days after treatment with estradiol, the proliferative response was suppressed in blood cultures stimulated with concanavalin A (P < 0.05) and phytohemagglutinin (P < 0.07). Effects of estradiol treatment were not found in any of the assays performed with purified BMC. We, therefore, assumed that in vivo exposure to estradiol can affect the function of porcine BMC; however, this was only evident when the in vitro assays were performed on blood cultures.