Schistosomiasis is a
parasitic infection caused by trematode worms (also called blood flukes) of the genus Schistosoma sp., which affects over 230 million people worldwide, causing 200,000 deaths annually. There is no
vaccine or new drugs available, which represents a worrying aspect, since there is loss of sensitivity of the parasite to the medication recommended by the World Health Organization,
Praziquantel. The present study evaluated the effects of the recombinant
enzymes of S. mansoni
Hypoxanthine-Guanine Phosphoribosyltransferase (
HGPRT),
Purine Nucleoside Phosphorylase (PNP) and the MIX of both
enzymes in the
immunotherapy of
schistosomiasis in murine model. These
enzymes are part of the
purine salvage pathway, the only metabolic pathway present in the parasite for this purpose, being essential for the synthesis of
DNA and
RNA. Female mice of Swiss and BALB/c strains were infected with cercariae and treated, intraperitoneally, with three doses of 100 µg of
enzymes. After the
immunotherapy, the eggs and adult worms were counted in the feces; the number of eosinophils from the fluid in the peritoneal cavity and peripheral blood was observed; and the quantification of the
cytokine IL-4 and the production of
antibodies IgE was analyzed. The evaluation of the number of
granulomas and
collagen deposition via histological slides of the liver was performed. The results demonstrate that
immunotherapy with the
enzyme HGPRT seems to stimulate the production of
IL-4 and promoted a significant reduction of
granulomas in the liver in treated animals. The treatment with the
enzyme PNP and the MIX was able to reduce the number of worms in the liver and in the mesenteric vessels of the intestine, to reduce the number of eggs in the feces and to negatively modulate the number of eosinophils. Therefore,
immunotherapy with the recombinant
enzymes of S. mansoni
HGPRT and PNP might contribute to the control and reduction of the pathophysiological aspects of
schistosomiasis, helping to decrease the morbidity associated with the
infection in murine model.