Chagas disease (CD), caused by the protozoa <i>Trypanosoma cruzi</i>, is a chronic illness in which parasites persist in the host-infected tissues for years.<i>T. cruzi</i> invasion in cardiomyocytes elicits the production of pro-inflammatory mediators [TNF-α, IL-1β, IFN-γ; nitric oxide (<sup>·</sup>NO)], leading to mitochondrial dysfunction with increased superoxide radical (O<sub>2</sub><sup>·-</sup>), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and peroxynitrite generation.
The severity of chronic chagasic cardiomyopathy (CCC), the most frequent clinical outcome of Chagas disease (CD), has been associated with cytokine-enriched heart tissue inflammation, and high serum levels of transforming growth factor (TGFβ), interferon-gamma (IFNγ), and tumour necrosis factor (TNF).
In this study we investigated the association of functional single nucleotide polymorphisms of tumor necrosis factor-alfa (TNFA) and TNF receptor 2 (TNFR2) genes in determining the susceptibility to Chagas' disease.
These results indicate that TNF polymorphisms are associated neither to CCC development nor to progression to more severe forms of cardiomyopathy in Brazilian Chagas disease patients.
We determined the TNFA (positions -308, -244 and -238) and TNFB genotypes in a sample of 85 serologically positive chagasic individuals and in 87 healthy controls from a Peruvian population where Trypanosoma cruzi infection is endemic.