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World J Cardiol. Aug 26, 2014; 6(8): 782-790
Published online Aug 26, 2014. doi: 10.4330/wjc.v6.i8.782
Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy
Ludmila Rodrigues Pinto Ferreira, Amanda Farage Frade, Monique Andrade Baron, Isabela Cunha Navarro, Jorge Kalil, Christophe Chevillard, Edecio Cunha-Neto
Ludmila Rodrigues Pinto Ferreira, Amanda Farage Frade, Monique Andrade Baron, Isabela Cunha Navarro, Jorge Kalil, Edecio Cunha-Neto, Laboratory of Immunology, Heart Institute (InCor), School of Medicine, University of São Paulo, 05403-001 São Paulo, Brazil
Ludmila Rodrigues Pinto Ferreira, Amanda Farage Frade, Monique Andrade Baron, Isabela Cunha Navarro, Jorge Kalil, Edecio Cunha-Neto, Division of Clinical Immunology and Allergy, School of Medicine, University of São Paulo, 05403-001 São Paulo, Brazil
Ludmila Rodrigues Pinto Ferreira, Amanda Farage Frade, Monique Andrade Baron, Isabela Cunha Navarro, Jorge Kalil, Edecio Cunha-Neto, Institute for Investigation in Immunology (iii), INCT, 05403-001 São Paulo, Brazil
Christophe Chevillard, Aix-Marseille Université, INSERM, GIMP UMR_S906, 13385 Marseille, France
Author contributions: Ferreira LRP prepared the multiple drafts and wrote the manuscript; Chevillard C and Cunha-Neto E prepared the framework of the article; Frade AF, Baron MA and Navarro IC helped with scientific discussions; Kalil J, Chevillard C and Cunha-Neto E improved the quality of the draft.
Correspondence to: Edecio Cunha-Neto, MD, PhD, Researcher, Associate Professor of Medicine, Laboratory of Immunology, Heart Institute (InCor), School of Medicine, University of São Paulo. Av. Dr. Eneas de Carvalho Aguiar, 44 BL 2, 9° andar, 05403-001 São Paulo, Brazil. edecunha@usp.br
Telephone: +55-11-26615906 Fax: +55- 11-26615953
Received: December 29, 2013
Revised: March 29, 2014
Accepted: May 31, 2014
Published online: August 26, 2014
Processing time: 261 Days and 16.4 Hours
Abstract

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.

Keywords: Chagas disease; Trypanosoma cruzi; Interferon-gamma; Gene expression; Cardiomyopathy

Core tip: Chagas disease cardiomyopathy (CCC) occurs in 30% of those infected with the protozoan Trypanosoma cruzi, endemic in Latin America. It is an inflammatory cardiomyopathy with a worse prognosis than cardiomyopathies of other etiologies. Interferon (IFN)- γ is the main cytokine produced locally and induces strong signaling in cardiomyocytes. This review focuses on the pleiotropic protective and pathogenic effects of IFN-γ on CCC.