cruzi infection. Interestingly, recent data support the idea that the CNS inflammation induced by acute stress is neuroprotective, at least for anxiety ( Lewitus et al., 2008). In our experiments, C57BL/6 mice were refractory to T. cruzi-induced CNS inflammation, whereas C3H/He mice presented acute phase-restricted meningoencephalitis with enrichment in CD8+ T-cells and macrophages ( Silva et al., 1999 and Roffê et al., 2003). Accordingly, the selective trafficking

of inflammatory cells to the CNS may explain the differential responses of the resistant C3H/He mice and susceptible C57BL/6 mice to T. cruzi-induced locomotor/exploratory alteration that may indicate anxiety; however, further studies are needed to determine the mechanism of this difference. Studies conducted in patients with chronic selleck chemicals llc Chagas disease have revealed the presence of cephalea, confusion and depression (Jorg and Rovira, 1981, Mangone et al., 1994 and Marchi et al., 1998). These data led us to investigate T. cruzi-induced depressive-like behavior in C3H/He and C57BL/6 mouse models that reproduce important pathological aspects of Chagas disease ( Medeiros et al., 2009, Silva et al., 2010 and Silverio et al., 2012). Notably, our experiments showed that, when infected with a low inoculum of the type I Colombian strain, neither mouse lineage presented sickness-related behavior. Moreover,

Daporinad clinical trial our results show that T. cruzi-infected C3H/He mice, which are susceptible to acute phase-restricted

CNS inflammation, exhibit depressive-like behavior during the acute and chronic phases of Silibinin infection. Therefore, this behavioral alteration was independent of active CNS inflammation, supporting the hypothesis that the chronic depressive-like behavior could be a long-term consequence of acute brain inflammation. However, T. cruzi-infected C57BL/6 mice, which are refractory to CNS inflammation, also displayed depressive-like behavior during the acute and chronic phases of infection. Thus, our findings suggest that T. cruzi-induced depression is independent of the active and previous trafficking of inflammatory cells to the CNS. Therefore, other biological mechanisms must explain the genesis of the chronic depression associated with T. cruzi infection. Given the genotypic and biological heterogeneity of T. cruzi strains ( Zingales et al., 2012), we attempted to clarify whether chronic depressive status was associated with the parasite strain infecting the host. Toward this end, we tested type I Colombian and type II Y T. cruzi strains, parasite prototypes that represent the strains most frequently found in nature ( Zingales et al., 2012). Infection with the type I Colombian strain led to acute (21, 30 dpi) and chronic (90, 120 and 150 dpi) depressive-like behavior in C3H/He mice. However, the enhanced immobility time due to infection with the type II Y T.