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Acta Trop. 2014 Nov;139:57-66. doi: 10.1016/j.actatropica.2014.07.005. Epub 2014 Jul 11.

Trypanosoma cruzi strains cause different myocarditis patterns in infected mice.

Author information

1
Instituto Venezolano de Investigaciones Científicas (IVIC), Caracas 1020A, Venezuela; Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain. Electronic address: hrodrigu@ivic.gob.ve.
2
Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain.
3
Fundación Jiménez Díaz, Servicio de Anatomía Patológica, Madrid, Spain.

Abstract

AIMS:

Chagas disease pathology is dependent on the infecting Trypanosoma cruzi strain. However, the relationship between the extent and type of myocarditis caused by different T. cruzi strains in the acute and chronic phases of infection has not been studied in detail. To address this, we infected mice with three genetically distant T. cruzi strains as well as infected in vitro different cell types.

METHODS AND RESULTS:

Parasitemia was detected in mice infected with the Y and VFRA strains, but not with the Sc43 strain; however, only the Y strain was lethal. When infected with VFRA, mice showed higher inflammation and parasitism in the heart than with Sc43 strain. Y and VFRA caused homogeneous pancarditis with inflammatory infiltrates along the epicardium, whereas Sc43 caused inflammation preferentially in the auricles in association with intracellular parasite localization. We observed intramyocardic perivasculitis in mice infected with the VFRA and Y strains, but not with Sc43, during the acute phase, which suggests that endothelial cells may be involved in heart colonization by these more virulent strains. In in vitro infection assays, the Y strain had the highest parasite-cell ratio in epithelial, macrophage and endothelial cell lines, but Y and VFRA strains were higher than Sc43 in cardiomyocytes.

CONCLUSIONS:

This study supports parasite variability as a cause for the diverse cardiac outcomes observed in Chagas disease, and suggests that endothelial cells could be involved in heart infection during the acute phase.

KEYWORDS:

Chagas disease; Myocarditis; T. cruzi

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