5b). There is evidence

that Schistosoma sp. infection protects humans [11] and AZD1208 concentration mice against allergic asthma [36,38,40]. We evaluated whether the S. mansoni antigens Sm22·6, PIII and Sm29 could down-modulate the inflammatory allergic response in a murine model of OVA-induced airway inflammation. We found that immunization with these S. mansoni antigens protected mice against allergic inflammation; there was a strong reduction in the number of inflammatory cells and eosinophils recruited to the airways. Moreover, the levels of OVA-specific IgE production were also decreased in mice immunized with Sm22·6, PIII and Sm29, and the levels of EPO in the lungs were lower in mice immunized with Sm22·6 and PIII, compared to the non-immunized mice. Additionally, we found that these two antigens have an important immunomodulatory effect on the production of the Th2 cytokines IL-4 and IL-5, evidenced by the lower levels of these cytokines in the BAL of immunized compared to non-immunized mice. IL-5 is a well-known cytokine that induces the production of eosinophils and activates these cells, while IL-4 acts on B cells, inducing

IgE synthesis. This antibody participates in the pathogenesis of asthma by binding to mast cells, basophils and eosinophils, which release inflammatory mediators upon contact with the allergen. We observed lower levels of allergen-specific IgE in the groups of S. mansoni antigen-immunized mice compared to non-immunized mice. This is additional evidence that these antigens are able to prevent Th2-mediated inflammation. In mice

immunized HM781-36B with Sm29, despite the fact that there was a reduction in the number Loperamide of inflammatory cells, eosinophils and OVA-specific IgE compared to non-immunized mice, the decrease in the levels of IL-4 and IL-5 in BAL did not reach statistical significance. The slight decrease in IL-4 and IL-5 production might be effective to reduce IgE production and eosinophils growth or recruitment without, however, being sufficient to alter EPO activity in lung tissue. We used the antigen IPSE as our positive control as this antigen is an inducer of the Th2 response in schistosomiasis [34]. As expected, in mice immunized with IPSE the Th2 parameters such as number of eosinophils, levels of EPO, IL-4 and IL-5 were comparable to asthmatic non-immunized mice; unpredictably, however, in IPSE-immunized mice there was a reduction in the levels of OVA-specific IgE. This study examined inflammatory mediators responsible for lung airway inflammation in a murine model of OVA-induced allergic asthma, and found an eosinophil infiltration of the airway. Eosinophils play a pivotal role in the airway inflammation in asthma and they correlate with the extent of inflammatory process in the lung parenchyma [41]. Lung function could not be evaluated in the present study.