**4. Conclusion**

Altogether, the findings of this study point that *T. cruzi* SC2005 strain can spread through the bloodstream and colonize different organs and tissues, producing a systemic response, which is variable depending on the inoculation route and the genetic background of the host. Heart and stomach were the most intensely parasitized and inflamed organs in all models. *T. cruzi* SC2005 strain infects preferentially the muscular layers of the organs, where inflammatory infiltrates are also observed with higher intensity, being associated with an increase and redistribution of collagen fibers. In the heart, inflammatory infiltrates are preferentially located in the atria, while parasites are mostly found in the ventricles.

*T. cruzi* SC2005 intragastric infection induces a hypochromic anemia, and an extramedullary hematopoiesis in mouse livers, characterized by the presence of immature cells and megakaryocytes, as well as an increase of CD4+ /CD8+ frequencies, corroborating the hypothesis that *T. cruzi* SC2005 infection causes an impairment in bone marrow function. Besides, the infection also induces a leukocytosis, characterized by an increase of CD8+ T lymphocytes, as well as an increase of proinflammatory cytokines production. The increase of leukocytes was correlated with the increase of parasitaemia.

The intraperitoneal infection proved to be more infective and severe than the intragastric route, leading to a higher parasitaemia, mortality, tissue colonization, and tissue inflammatory response.

The mouse strain influences the immune response, pointing to a role for host genetics in the susceptibility to infection. In this study, although *T. cruzi* SC2005 intragastric infection has been induced a similar profile of changes in A and BALB/c mice, the earlier development of a proinflammatory cytotoxic cellular profile of A mice led to a less severe disease outcome, with lower parasite load and mortality. Infected A mice also exhibited an early induction of CD8+ T cells and proinflammatory cytokine production. On the other hand, for BALB/c-infected mice the response to infection occurred later, after a considerable increase in parasitemia, favoring the parasite multiplication and spread, and consequent higher mortality rate and tissue inflammation.

This study adds highlights on the factors that influence the pathology of Chagas disease, helping in the understanding of its different outcomes.
