The latter data are compatible with other results obtained using the same experimental model (15,16). Our work also demonstrates that, upon challenge,
the increase in IgE production and eosinophil infiltration in the skin and lung was already detected at 7 days of infection. However, these responses showed an earlier onset in the experimental groups that were previously infected with a high-dose of infective larvae (L500). Given the fact that the L10 group had a similar protection rate as the L500 group on day 2, it is likely that eosinophilic inflammation was not essential for the destruction of migrating larvae during challenge infection with S. venezuelensis as was shown by Galioto et al. whereby S. stercoralis larvae control mechanisms in immunized selleck chemicals mice were independent of eosinophils (38). Moreover, early induction of IL-4 was similarly detected in both experimental groups (L10 and L500), suggesting that other IL-4-dependent mechanisms could be involved in larvae control during challenge infection. Animals from the L500 group maintained elevated production
of IL-4, with only a slight increase in IFN-γ during the intestinal phase of the challenge infection with S. venezuelensis, whereas the L10 group showed increased production of both, IL-4 (type-2 cytokine) and IFN-γ (type-1cytokine). The absence of polarization to type-2 immune response in mice previously
infected with a low number of larvae is suggested based on the mixed cytokine profile and to the lower eosinophil infiltration, IKBKE which could CHIR-99021 purchase account for the delay in adult worm elimination during challenge infection. This observation is supported by a previous study by Fernandes et al., in which mice that were primed with soluble larvae antigen and subsequently underwent a challenge with S. venezuelensis live larvae were not able to eliminate the parasites completely from the intestine, possibly because of the mixed Th1/Th2 response (24). Other studies using Trichuris muris have also shown that low antigen doses tended to give a mixed Th1/Th2 response (39). Alternatively, our data could suggest stronger induction of regulatory T cells during challenge infection in low-dose (L10), leading to lower cellular infiltration. Research based on regulatory T cells and helminth infections have indicated that some parasites may induce CD4+CD25+FoxP3+ cells in the infected host, consequently modulating effector mechanisms – such as type 2 polarization – thereby allowing worm survival (40).The participation of regulatory T cells in S. venezuelensis survival has not been assessed here; however, it is important to notice that low-dose priming group did show increased level of IFN-γ upon challenge infection.