The present study was aimed at pathologically and immunohistochemically evaluating the effects of interferon gamma (IFN-g) and aminoguanidine (AG) in rats experimentally infected with Fasciola hepatica. A total of 44 Wistar rats were divided into 4 groups. With the exception of the controls (fourth group), the remaining rats were infected orally with 25 metacerceria of F. hepatica. The first group was administered 0.2% AG in drinking water daily, in order to block nitric oxide (NO) production. The second group was administered 250 units of IFN-g daily, in order to stimulate NO synthesis. The third group was administered a placebo only. At the end of the 2 month experimentation period all the rats were killed under ether anesthesia and necropsied. Migrating tracts, necrosis, and enlargement of the main bile duct were the predominant lesions in infected livers. The parasite burden was lower in the IFN-g-treated rats than rats in the other groups. Acute migrating tracts were occluded with numerous erythrocytes, necrotic hepatocytes, and neutrophils and surrounded by mononuclear cell infiltration interspersed with eosinophils. Chronic migrating tracts were generally repaired with fibrous connective tissue and surrounded by chronic inflammatory infiltrate. Immunohistochemistry detected CD3+ T and CD79acy + B lymphocyte infiltration, l IgG + plasmocytes and PCNA-positive cells in the infected livers, hepatic and mesenterial lymph nodes, and Peyer's patches. Given the low numbers of parasites and the limited repair in the liver of the animals administered IFN-g and the severity of the lesions in the livers of the animals administered AG, it was concluded that IFN-g positively affected the immune system and that AG blocked NO production in the animals.
The present study was aimed at pathologically and immunohistochemically evaluating the effects of interferon gamma (IFN-g) and aminoguanidine (AG) in rats experimentally infected with Fasciola hepatica. A total of 44 Wistar rats were divided into 4 groups. With the exception of the controls (fourth group), the remaining rats were infected orally with 25 metacerceria of F. hepatica. The first group was administered 0.2% AG in drinking water daily, in order to block nitric oxide (NO) production. The second group was administered 250 units of IFN-g daily, in order to stimulate NO synthesis. The third group was administered a placebo only. At the end of the 2 month experimentation period all the rats were killed under ether anesthesia and necropsied. Migrating tracts, necrosis, and enlargement of the main bile duct were the predominant lesions in infected livers. The parasite burden was lower in the IFN-g-treated rats than rats in the other groups. Acute migrating tracts were occluded with numerous erythrocytes, necrotic hepatocytes, and neutrophils and surrounded by mononuclear cell infiltration interspersed with eosinophils. Chronic migrating tracts were generally repaired with fibrous connective tissue and surrounded by chronic inflammatory infiltrate. Immunohistochemistry detected CD3+ T and CD79acy + B lymphocyte infiltration, l IgG + plasmocytes and PCNA-positive cells in the infected livers, hepatic and mesenterial lymph nodes, and Peyer's patches. Given the low numbers of parasites and the limited repair in the liver of the animals administered IFN-g and the severity of the lesions in the livers of the animals administered AG, it was concluded that IFN-g positively affected the immune system and that AG blocked NO production in the animals.
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