Chaga's disease caused by infection with Trypanosoma cruzi leads to a miocardiopathy that evolves from the acute to the chronic phase. Although several hypotheses have been raised to explain the pathogenesis of chagasic myocardiopathy, its main molecular pathway remains unsolved. T. cruzi express on its surface and shed a virulent factor, the trans-sialidase (TS) enzyme, involved in the innate and acquired host immunity. In this work we employed flow cytometry, histopathology and imunohistochemistry to assess the effects of TS from T. cruzi on expression of adhesion molecules (LFA-1, VLA-4, CD62L and CD43), activation markers (CD44 and CD69) and homing of T cells subsets isolated from the hearts of T. cruzi infected mice. Mice C57BL6 were infected with 10⁴ blood trypomastigotes (Y strain) and treated with 30 µg of TS one hour before infection, as well as at day 2 and 3 post-infection. Control mice were treated with PBS. The blood trypomastigotes were evaluated at days 6-10, and the hearts were processed and examined at day 15 post-infection. We show that TS-treated mice present a significant increase on the number of blood trypomastigotes. The histopathological analyses show that the cardiac tissue of TS-treated mice presents a diffuse inflammatory focus, with a significant enrichment of leukocytes by area (20 mm²). Although, the imunohistochemistry and flow cytometry studies revealed no alteration on the percentage of infiltrating T cells, TS-treated mice present a significant increase of CD8 T cells displaying an activated phenotype (CD8⁺/CD44₊), characteristic for effector-memory T cells. Therefore our results suggest a role for TS in the inflammatory damage caused by the presence of CD8(+) T cells in the cardiac tissue during T. cruzi infection.