Nitric Oxide Donors with Therapeutic Strategic in Experimental Schistossomiasis Mansoni

Schistosomiasis, an immune disease, remains a major public health problem in endemic area. To determine the influence of Nitric Oxide (NO) on this disease, the auhtors tested two compounds (Trans-(Ru(bpy) sub( 2)(NO)SO3)(PF sub( 6))-PF sub( 6) and Na sub( 2)(Fe(CN) sub( 5)(NO))-SNP, which releases N...

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Veröffentlicht in:American journal of immunology 2014, Vol.10 (4), p.225-239
Hauptverfasser: Silva, Jean Jerley Nogueira da, Pavanelli, Wander Rogério, Panis, Carolina, Cunha, Thiago Mattar, Oliveira, Francisco José de Abreu, Menezes, Maria Claudia Noronha Dutra de, Costa, Ivete Conchon, Thomé, Graciele da Silva, Silva, Francisco Ordelei Nascimento da, Sousa, Eduardo Henrique Silva de, Lopes, Luiz Gonzaga de França, Cecchini, Rubens, Cunha, Fernando de Queiroz, Itano, Eiko Nakagawa, EharaWatanabe, Maria Angélica
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Sprache:eng
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Zusammenfassung:Schistosomiasis, an immune disease, remains a major public health problem in endemic area. To determine the influence of Nitric Oxide (NO) on this disease, the auhtors tested two compounds (Trans-(Ru(bpy) sub( 2)(NO)SO3)(PF sub( 6))-PF sub( 6) and Na sub( 2)(Fe(CN) sub( 5)(NO))-SNP, which releases NO when activated by biological reducing agents, in BALB/c mice infected subcutaneously by Schistosoma BH strains. They found that NO-donors treated mice were more resistant to infection, since they exhibited higher survival. Furthermore, they observed in histopathological analysis a decreased influx of inflammatory cells in the hepatic tissue of mice treated with both donors. The parasite counting was also minor in treated mice. Moreover, decreased levels of IL-10 were detected in the liver of infected mice treated with SNP. The animals treated with PF sub( 6) showed high plasmatic NO levels at 45 days after infection. Altogether, these data suggest that NO is a pivotal factor of resistance during schistossomiasis by controlling parasites proliferation, influencing cytokine production and consequently modulating the development of inflammatory response.
ISSN:1553-619X
1558-3775
DOI:10.3844/ajisp.2014.225.239