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Published on: September 30, 2017
Changes in cellular contractility and cytokines profile during Trypanosoma cruzi infection in mice
Danilo Roman-Campos1, Hugo Leonardo L Duarte, Policarpo A Sales
1Dept. of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Insights
Chagas
Area of Science:
- Cardiology
- Parasitology
- Immunology
Background:
- Chagas' disease, caused by Trypanosoma cruzi, leads to heart failure and dilated cardiomyopathy.
- Cardiac myocyte contractility changes during Chagas' disease are poorly understood.
- Investigating the link between parasite infection and cardiac function is crucial.
Purpose of the Study:
- To investigate the relationship between T. cruzi infection, cytokine profiles, and cardiac myocyte contractility.
- To characterize alterations in cellular contractility during acute and chronic phases of experimental Chagas' disease.
Main Methods:
- Infection of mice with Trypanosoma cruzi.
- Evaluation of cardiac myocyte contractility (fractional shortening, contraction/relaxation times, velocities).
- Measurement of circulating cytokines (IFN-gamma, TNF-alpha, MCP-1/CCL2).
Main Results:
- Cardiac myocyte contractility was altered in all three heart regions studied.
- Slower contraction/relaxation times and velocities were observed during both acute and chronic phases.
- Altered contractility correlated with elevated IFN-gamma, TNF-alpha, and MCP-1/CCL2 levels.
Conclusions:
- Cardiac myocyte contractility is impaired early in T. cruzi infection and persists into the chronic phase.
- IFN-gamma, TNF-alpha, and MCP-1/CCL2 play a role in mechanical heart remodeling in experimental Chagas' disease.
- Findings highlight the impact of inflammation on cardiac function during Chagas' disease.
Abstract:
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-gamma, TNF-alpha 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-gamma, TNF-alpha and MCP-1/CCL2 in the mechanical heart remodeling during experimental Chagas' disease.
