The effects of using nitric oxide (NO) donors and inhibitors in experimental strongyloidiasis were showed using, both naïve and dexamethasone immunosuppressed BALB/c mice infected with Strongyloides venezuelensis. Aminoguanidine, an inhibitor of inducible NO synthase and LA419 a NO donor, were administered. Dexamethasone was used to induce immunosuppression. The study in BALB/c mice revealed increases in counts of fecal eggs, larvae in lungs and parasitic females following treatment with aminoguanidine, while mice treated with LA419 had limited egg output with low larval and adult recoveries. Mice immunosuppressed with dexamethasone developed hyperinfection with high long lasting fecal egg emission, high numbers of larvae in lungs and high numbers of parasitic females in the intestine even when the infection had already been cleared in non-immunosuppressed infected controls. Mice treated with dexamethasone and aminoguanidine had the highest egg output and the highest larva and parasitic female recovery showing a severe hyperinfection syndrome. In contrast, treatment with dexamenthasone and LA419 resulted in a controlled hyperinfection syndrome and these mice were able to eliminate the parasite. Therefore, NO modulation appears to be a determinant factor in severe strongyloidiasis and further studies should be conducted to confirm in other experimental models.
Keywords: Aminoguanidine; Dexamethasone; Hyperinfection syndrome; LA419; Nitric oxide; Strongyloides venezuelensis.
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