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Memórias do Instituto Oswaldo Cruz
Fundação Oswaldo Cruz, Fiocruz
ISSN: 1678-8060
EISSN: 1678-8060
Vol. 104, No. s1, 2009, pp. 252-258
Bioline Code: oc09114
Full paper language: English
Document type: Research Article
Document available free of charge

Memórias do Instituto Oswaldo Cruz, Vol. 104, No. s1, 2009, pp. 252-258

 en Immunological and Non-Immunological Effects of Cytokines and Chemokines in the Pathogenesis of Chronic Chagas Disease Cardiomyopathy
Cunha-Neto, Edecio; Nogueira, Luciana G.; Teixeira, Priscila C.; Ramasawmy, Rajendranath; Drigo, Sandra A.; Goldberg, Anna Carla; Fonseca, Simone G.; Bilate, Angelina M. & Kalil, Jorge


The pathogenesis of Chagas disease cardiomyopathy (CCC) is not well understood. Since studies show that myocarditis is more frequent during the advanced stages of the disease, and the prognosis of CCC is worse than that of other dilated cardiomyopathies of non-inflammatory aetiology, which suggest that the inflammatory infiltrate plays a major role in myocardial damage. In the last decade, increasing evidence has shown that inflammatory cytokines and chemokines play a role in the generation of the inflammatory infiltrate and tissue damage. CCC patients have an increased peripheral production of the inflammatory Th1 cytokines IFN-γ and TNF-α when compared to patients with the asymptomatic/indeterminate form. Moreover, Th1-T cells are the main producers of IFN-γ and TNF-α and are frequently found in CCC myocardial inflammatory infiltrate. Over the past several years, our group has collected evidence that shows several cytokines and chemokines produced in the CCC myocardium may also have a non-immunological pathogenic effect via modulation of gene and protein expression in cardiomyocytes and other myocardial cell types. Furthermore, genetic polymorphisms of cytokine, chemokine and innate immune response genes have been associated with disease progression. We will review the molecular and immunological mechanisms of myocardial damage in human CCC in light of recent findings.

Chagas disease cardiomyopathy - cytokines - chemokines - gene polymorphism - energy metabolism

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