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2099-12-31
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CHANGES IN CELLULAR CONTRACTILITY AND CYTOKINES PROFILE DURING TRYPANOSOMA CRUZI INFECTION IN MICE
chagas' disease
cellular contractility
cytokines
chemokines
cardiac chambers
heart failure
Author
Affilliation
Dept. of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil/Hospital Santa Casa de Misericórdia de Belo Horizonte. Núcleo de Pós-Graduação e Pesquisa. Belo Horizonte, MG, Brazil
Universidade Federal de Viçosa. Belo Horizonte, MG, Brazil
Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Excitable Membranes and Cardiovascular Biology. Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil/Hospital Santa Casa de Misericórdia de Belo Horizonte. Núcleo de Pós-Graduação e Pesquisa. Belo Horizonte, MG, Brazil
Universidade Federal de Viçosa. Belo Horizonte, MG, Brazil
Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Immunopathology. René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil/Laboratory of Excitable Membranes and Cardiovascular Biology. Dept. of Biochemistry and Immunology. Universidade Federal de Minas Gerais. Belo Horizonte, MG, Brazil
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
Keywords
Trypanosoma cruzichagas' disease
cellular contractility
cytokines
chemokines
cardiac chambers
heart failure
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