TY - JOUR AU - Pavanelli, Wander Rogério AU - da Silva, Jean Jerley Nogueira AU - Panis, Carolina AU - Cunha, Thiago Mattar AU - Oliveira, Francisco José Abreu AU - Menezes, Maria Claudia Noronha Dutra de AU - Costa, Ivete Conchon AU - Thomé, Graciele da Silva AU - Silva, Francisco Ordelei Nascimento da AU - Sousa, Eduardo Henrique Silva de AU - Lopes, Luiz Gonzaga França AU - Cecchini, Rubens AU - Cunha, Fernando Queiroz AU - Itano, Eiko Nakagawa AU - EharaWatanabe, Maria Angélica PY - 2015 TI - Nitric Oxide Donors with Therapeutic Strategic in Experimental Schistossomiasis Mansoni JF - American Journal of Immunology VL - 10 IS - 4 DO - 10.3844/ajisp.2014.225.239 UR - https://thescipub.com/abstract/ajisp.2014.225.239 AB - Schistosomiasis, an immune disease, remains a major public health problem in endemic area. To determine the influence of Nitric Oxide (NO) on this disease, we tested two compounds (Trans-[Ru(bpy)2(NO)SO3](PF6)-PF6 and Na2[Fe(CN)5(NO)]-SNP, which releases NO when activated by biological reducing agents, in BALB/c mice infected subcutaneously by Schistosoma BH strains. The parasitic activity of NO-donors was evaluated in this model by measuring the immune cellular response in liver with: Cytokines levels; histopathological characteristics and the number of the granulomatous lesions; and NO levels. We found that NO-donors treated mice were more resistant to infection, since they exhibited higher survival. Furthermore, we observed in histopathological analysis a decreased influx of inflammatory cells in the hepatic tissue of mice treated with both donors. The parasite counting (estimated as eggs and worms number) 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 PF6 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.