Open AccessInterferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy
Author(s) -
Ludmila Rodrigues Pinto Ferreira,
Amanda Farage Frade,
Monique Baron,
Isabela Cunha Navarro,
Jorge Kalil,
Christophe Chevillard,
Edécio CunhaNeto
Publication year - 2014
Publication title -
world journal of cardiology
Language(s) - English
Resource type - Journals
ISSN - 1949-8462
DOI - 10.4330/wjc.v6.i8.782
Subject(s) - myocarditis , medicine , trypanosoma cruzi , chagas disease , cardiomyopathy , inflammation , heart failure , immunology , pathological , interferon , disease , parasite hosting , world wide web , computer science
Chagas disease cardiomyopathy (CCC), the main consequence of Trypanosoma cruzi (T.cruzi) infection, is an inflammatory cardiomyopathy that develops in up to 30% of infected individuals. The heart inflammation in CCC patients is characterized by a Th1 T cell-rich myocarditis with increased production of interferon (IFN)-γ, produced by the CCC myocardial infiltrate and detected at high levels in the periphery. IFN-γ has a central role in the cardiomyocyte signaling during both acute and chronic phases of T.cruzi infection. In this review, we have chosen to focus in its pleiotropic mode of action during CCC, which may ultimately be the strongest driver towards pathological remodeling and heart failure. We describe here the antiparasitic protective and pathogenic dual role of IFN-γ in Chagas disease.