Abstract
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.
Highlights
Schistosoma mansoni is an important helminth parasite
We have previously demonstrated that mice treated with Cis-[Ru(bpy)2(NO)SO3](PF6) are more resistant to Paracoccidioidomycosis (PCM) infection, presenting prolonged survival with reduced leukocyte recruitment and TNF-α production in the lung and liver as well as increased production of the anti-inflammatory cytokine IL-10 (Pavanelli et al, 2011)
We observed that 80% of infected mice treated with the donors survived up to 60 days p.i., the mortality of the infected mice treated with vehicle was only of 40%, with initiation on day 25 p.i., (Fig. 1)
Summary
Schistosoma mansoni is an important helminth parasite. During its course of infection, different stages of S. mansoni cause markedly varied patterns of inflammatory responses in hosts. The etiopathogenesis associated with schistosomiasis is largely attributed to the intense granulomatous inflammatory response and subsequent fibrosis induced by parasite eggs that become trapped in host organs such as the liver and intestine. Decreased fibrosis in the murine model is associated with diminished production of Th2 cytokines and increased production of Th1 cytokines (Cheever et al, 2002). Modulation of both Th1 and Th2 responses
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
