RESUMO
Trypanosoma cruzi (T. cruzi) and Toxoplasma gondii (T. gondii) are the causative agents of Chagas disease and Toxoplasmosis. T. cruzi and T. gondii present, respectively, low and high congenital transmission rates and induce a distinctive cytokine/chemokine profile in ex vivo infected human placental explants (HPE). Since the innate immune response is regulated, at least partially, by NF-κB signaling pathways, our main objective was to determine the effect of ex vivo infection with both parasites on the activation of canonical and non-canonical NF-κB pathways and its relation to parasite infection. T. cruzi activates both, the canonical and non-canonical pathways of NF-κB, unlike T. gondii, which has no effect on the canonical pathway and inhibits the non-canonical pathway. The inhibition of both pathways of NF-κB increases the DNA load of T. cruzi and T. gondii in HPE. Therefore, the differential modulation of NF-κB signal transduction pathways by both parasites might explain, at least partially, the low and high congenital transmission rates of T. cruzi and T. gondii.
