Changes in cellular contractility and cytokines profile during Trypanosoma cruzi infection in mice

• Autor(a) principal: Natali, Antonio J.
• Data de Publicação: 2009
• Outros Autores: Duarte, Hugo Leonardo L., Sales Jr, Policarpo A., Ropert, Catherine, Gazzinelli, Ricardo T., Cruz, Jader S., Roman-Campos, Danilo
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: LOCUS Repositório Institucional da UFV
• Texto Completo: https://doi.org/10.1007/s00395-009-0776-x; http://www.locus.ufv.br/handle/123456789/22761
• topic: Trypanosoma cruzi; Chagas’ disease; Cellular contractility; Cytokines; Chemokines; Cardiac chambers; Heart failure

Trypanosoma cruzi, an intracellular protozoan parasite infecting a wide variety of vertebrates, is the agent responsible for Chagas’ disease. This pathology often results in severe inflammatory heart condition and it is one of the major causes of dilated cardiomyopathy leading to heart failure in Latin America. Nevertheless, little is known about the changes in isolate cardiac myocytes contractility during the development of this pathology. Here we report a relationship between cytokines profile of mice infected with T. cruzi and the modifications in the cellular contractility pattern. We found that cellular contractility, measured as fractional shortening, showed a complex behavior. The changes were evaluated during the acute phase (15, 30 and 45 dpi) and chronic phase (>90 dpi). The time to half contraction and relaxation were lengthier despite the number of days after infection or the heart region evaluated. The maximal contraction and relaxation velocities were significantly slower. The observed changes in cellular contractility were correlated with the presence of circulating IFN-γ, TNF-α and MCP-1/CCL2 during the course of infection. Together, our data demonstrate that cellular contractility is altered in the three heart regions studied, and these alterations are observed at the very beginning of the parasitism and they remained until the chronic phase has been reached. Indeed, we propose a role for IFN-γ, TNF-α and MCP-1/CCL2 in the mechanical heart remodeling during experimental Chagas’ disease.