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Activation of rat splenic macrophage and lymphocyte functions by fumonisin B1

Author:
Dombrink-Kurtzman, M.A., Gomez-Flores, R., Weber, R.J.
Source:
Immunopharmacology 2000 v.49 no.3 pp. 401
Subject:
mycotoxicosis, immune response, macrophage activation, spleen, T-lymphocytes, cell proliferation, rats, animal disease models, Gibberella fujikuroi, Fusarium proliferatum, animal pathogenic fungi, fumonisin B1, mycotoxins, food contamination, feed contamination, dose response, interferons, nitric oxide, signal transduction, interleukin-2, human health, animal health, interferon-gamma
Abstract:
Fumonisins represent a family of toxic, structurally related metabolites produced by fungi that are found in corn worldwide. We investigated the effects of the mycotoxin, fumonisin B1, on rat splenic macrophage and lymphocyte functions. Pretreatment (24 h) of resident macrophages with fumonisin B1 (1, 10, and 100 μg/ml) significantly (p<0.01) stimulated nitric oxide production (0.48, 2.60, and 4.40 nmol nitrite/well, respectively), compared with the response of untreated macrophages (no nitrite detected), after 72 h of culture. Fumonisin B1 (1 and 10 μg/ml) and IFN-γ acted in an additive manner to activate nitric oxide production. The response of IFN-γ (50 U/ml)-activated macrophages (1.68 nmol nitrite/well) was potentiated (3.52, 4.96, and 4.44 nmol nitrite/well) by fumonisin B1 (1, 10, and 100 μg/ml, respectively). In addition, fumonisin B1 significantly (p<0.05) potentiated Con A (1.25 to 5 μg/ml) (1.46- to 2.62-fold increases)- and antiTCR, IL-2 or antiTCR+IL-2 (1.72- to 2.60-fold increases)-induced proliferation of splenic cells in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (NMA). These results show two distinct and separate effects of fumonisin B1: it induces nitric oxide production by macrophages and it stimulates T cell proliferation.
Agid:
3258
Handle:
10113/3258