Furthermore comparing the eNOS expression in both groups we observed a reduction in mesenteric endothelial cells from infected compared to control mice, with no alteration of caveolin-1 expression, a known repressor of eNOS activity. Finally, the number of basal adherent leukocytes to mesenteric endothelial cells in our model was similar to previous data in mesenteric vessels of eNOS-deficient mice. All evidence of the current model reinforce the important role of eNOS to the integrity of the microcirculatory endothelial barrier in vivo, as observed in other experimental models. Most probably there may be other phenotypic alterations of endothelial cells not addressed in this work that also contribute to the increased leukocyte adhesion. Therefore, firstly we propose that the increased endothelial cell-leukocyte interaction, and probably vascular permeability, in murine schistosomiasis are partially related to the reduced eNOS expression. Additionally, the mesenteric endothelial cells of infected mice keep in culture the phenotypic profile of their donor animal as described elsewhere. Consequently, it is herein suggested that schistosomiasis primes murine endothelial cells so that they keep the information of increasing leukocyte adhesion in culture, making endothelial cells culture a putative model to study in vitro the consequences of the disease. The mediator involved in the reduction of eNOS expression in this model has not been identified so far, and is beyond the scope of the present study. However, the disease provides a repertoire of modulators for the host immune system. Hence, it is reasonable to suppose that the reduced expression of eNOS may reflect the balance of the effects of parasite-derived molecules and host cytokines, i.e., an integrated network of biological events, rather than the effect of a single mediator. In summary, our data show that murine schistosomiasis increases vascular permeability and leukocyte-endothelial interaction while reduces the expression of eNOS, promoting an inflamed cellular profile in peritoneum. Additionally, mesenteric endothelial cells from S. mansoni-infected mice suffer a phenotypic change that is maintained in culture suggesting that the disease probably triggers epigenetic regulation of endothelial cells. Hepatoblastoma has an incidence of 0.6 per 100,000 children. Improved outcome was achieved through clinical trials such as the Childhood Liver Dabrafenib cost Tumours Strategy Group and the study HB 89–99 of GPOH.