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DTU I isolates of Trypanosoma cruzi induce upregulation of Galectin-3 in murine myocarditis and fibrosis

Published online by Cambridge University Press:  13 February 2014

MARÍA F. FERRER
Affiliation:
Instituto de Biotecnología y Biología Molecular, Universidad Nacional de La Plata, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina
CARLA A. PASCUALE
Affiliation:
Instituto de Microbiología y Parasitología Médica, Universidad de Buenos Aires-CONICET, Argentina Instituto de Investigaciones Biotecnológicas, Instituto Tecnológico de Chascomús, Universidad Nacional de San Martin-CONICET, Argentina
RICARDO M. GOMEZ*
Affiliation:
Instituto de Biotecnología y Biología Molecular, Universidad Nacional de La Plata, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina
MARÍA S. LEGUIZAMÓN*
Affiliation:
Instituto de Microbiología y Parasitología Médica, Universidad de Buenos Aires-CONICET, Argentina Instituto de Investigaciones Biotecnológicas, Instituto Tecnológico de Chascomús, Universidad Nacional de San Martin-CONICET, Argentina
*
* Corresponding authors. Ricardo M. Gómez, Instituto de Biotecnología y Biología Molecular, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Calle 49 y 115, 1900 La Plata, Argentina. E-mail: rmg@biol.unlp.edu.ar
* María Susana Leguizamón, Instituto de Microbiología y Parasitología Médica, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Piso 13, 1121, Buenos Aires, Argentina. E-mail: sleguiza@fmed.uba.ar

Summary

Chagas heart disease is a major public concern since 30% of infected patients develop cardiac alterations. The relationship between Trypanosoma cruzi discrete typing units (DTUs) and the biological properties exhibited by the parasite population has yet to be elucidated. In this study, we analysed the expression of α-smooth muscle actin (α-SMA) and galectin-3 (Gal-3) associated with cardiac extracellular matrix (ECM) remodelling a murine chronic cardiomyopathy induced by Tc I genotypes. We found the induction of myocarditis was associated with the upregulation of Col I, α-SMA, Gal-3, IFN-γ and IL-13, as analysed by q-PCR. In myocardial areas of fibrosis, the intensity of myocarditis and significant ECM remodelling correlated with the presence of Col I-, Gal-3- and α-SMA-positive cells. These results are promising for the further efforts to evaluate the relevance of Gal-3 in Chagas heart disease, since this galectin was proposed as a prognosis marker in heart failure patients.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2014 

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