Effects of iNOS inhibitor on IFN-gamma production and apoptosis of splenocytes in genetically different strains of mice infected with Toxoplasma gondii
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Abstract
To evaluate the effects of nitric oxide (NO) on IFN-γ production and apoptosis induction in genetically different strains of mice with toxoplasmosis, BALB/c (a toxoplasmosis resistant strain) and C57BL/6 (a toxoplasmosis susceptible strain) mice were administered T. gondii cysts orally and injected intraperitoneally with aminoguanidine, an iNOS inhibitor (AG; 35 mg/kg per mouse daily for 14 days). No deaths occurred among the AG treated BALB/c mice administered T. gondii, whereas infected and AG-treated C57BL/6 mice survived only a few days. The numbers of brain cysts were significantly greater and the NO and IFN-γ levels in splenocyte culture supernatants were significantly lower in infected and AG-treated C57BL/6 mice than in the infection controls, whereas infected and AG-treated BALB/c mice had parasite burdens, and NO and IFN-γ levels that were similar to those of the infected controls.The apoptotic splenocyte fractions in the infected and AG-treated groups of both mouse strains were not significantly different from those in the infected non-treated controls. These results suggest that NO modulates IFN- production in T. gondii-infected C57BL/6 mice, and that NO is involved in mediating a protective response in toxoplasmosis susceptible mouse strain during acute infection. However, this suggested effect was not apparent in the toxoplasmosis resistant strain.
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