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Blood Gene Signatures of Chagas Cardiomyopathy With or Without Ventricular Dysfunction
Ludmila Rodrigues Pinto Ferreira1,2,3,4, Frederico Moraes Ferreira1,2,3,4, Helder Imoto Nakaya5,6
1Laboratory of Immunology and.
Insights
Chagas disease progression involves distinct gene expression profiles, particularly in chronic Chagas cardiomyopathy (CCC). Natural killer/CD8+ T-cell cytotoxicity pathways are key differentiators between CCC patient groups, offering insights into disease mechanisms.
Area of Science:
- Cardiovascular Disease
- Infectious Disease
- Genomics
Background:
- Chagas disease, caused by Trypanosoma cruzi, impacts 7 million people, with 30% developing chronic Chagas cardiomyopathy (CCC).
- Understanding the molecular mechanisms driving CCC progression is crucial for developing effective treatments.
- Transcriptome analysis offers a powerful tool for identifying molecular changes associated with disease outcomes.
Purpose of the Study:
- To investigate whole-blood gene expression profiles in patients with Chagas disease.
- To identify molecular differences between asymptomatic Chagas disease and chronic Chagas cardiomyopathy (CCC) with varying left ventricular ejection fraction (LVEF).
- To explore the role of specific gene expression patterns, particularly those related to immune cell activity, in CCC progression.
Main Methods:
- Whole-blood transcriptome analysis using microarray on 150 subjects (30 controls, 120 Chagas disease patients).
- Chagas disease patients were categorized into asymptomatic, CCC with preserved LVEF, and CCC with reduced LVEF groups.
- Differential gene expression analysis and functional pathway profiling were performed.
Main Results:
- Distinct gene expression and functional pathway profiles were observed across different Chagas disease groups.
- Significant differences in gene expression were most pronounced between CCC groups with preserved and reduced LVEF.
- A set of 27 differentially expressed genes, primarily linked to natural killer (NK)/CD8+ T-cell cytotoxicity, distinguished these two CCC groups.
Conclusions:
- Gene expression patterns in Chagas disease, especially CCC, vary significantly based on disease severity and cardiac function.
- Natural killer (NK)/CD8+ T-cell cytotoxicity appears to be a critical factor in differentiating the progression of Chagas cardiomyopathy.
- Identifying these key genes may enhance our understanding of CCC pathogenesis and aid in the development of prognostic markers.
Abstract:
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 7 million people in Latin American areas of endemicity. About 30% of infected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, and myocarditis. Further studies are necessary to understand the molecular mechanisms of disease progression. Transcriptome analysis has been increasingly used to identify molecular changes associated with disease outcomes. We thus assessed the whole-blood transcriptome of patients with Chagas disease. Microarray analysis was performed on blood samples from 150 subjects, of whom 30 were uninfected control patients and 120 had Chagas disease (1 group had asymptomatic disease, and 2 groups had CCC with either a preserved or reduced left ventricular ejection fraction [LVEF]). Each Chagas disease group displayed distinct gene expression and functional pathway profiles. The most different expression patterns were between CCC groups with a preserved or reduced LVEF. A more stringent analysis indicated that 27 differentially expressed genes, particularly those related to natural killer (NK)/CD8+ T-cell cytotoxicity, separated the 2 groups. NK/CD8+ T-cell cytotoxicity could play a role in determining Chagas disease progression. Understanding genes associated with disease may lead to improved insight into CCC pathogenesis and the identification of prognostic factors for CCC progression.
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