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Updated: Aug 8, 2025
In Vitro Drug Screening Against All Life Cycle Stages of Trypanosoma cruzi Using Parasites Expressing β-galactosidase
Published on: November 5, 2021
Cytokine Networks as Targets for Preventing and Controlling Chagas Heart Disease
Carolina Cattoni Koh1, Eula G A Neves1, Thaiany Goulart de Souza-Silva1
1Laboratório de Biologia das Interações Celulares, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, MG, Brazil.
Insights
Chagas disease, caused by Trypanosoma cruzi, affects millions. Immune responses and gene variations influence whether patients develop severe cardiac issues, offering potential disease control targets.
Area of Science:
- Immunology
- Infectious Diseases
- Genetics
Background:
- Chagas disease, caused by Trypanosoma cruzi, is a major health concern in Latin America, with increasing cases globally.
- The disease has an indeterminate asymptomatic phase and a severe cardiac form affecting approximately 30% of patients.
- Distinct immune responses differentiate clinical outcomes, highlighting the need to understand disease pathogenesis.
Purpose of the Study:
- To review the association between chemokines, cytokines, cytotoxic molecules, and clinical outcomes in human Chagas disease.
- To explore the role of gene polymorphisms in regulating these immunomodulatory molecules.
- To discuss the potential of these factors as biomarkers for disease susceptibility and targets for control.
Main Methods:
- Review of existing studies on human Chagas disease.
- Analysis of associations between immune mediators and clinical manifestations.
- Examination of the impact of gene polymorphisms on immune responses.
Main Results:
- Chemokines, cytokines, and cytotoxic molecules are linked to distinct clinical outcomes in Trypanosoma cruzi infection.
- Gene polymorphisms influence the transcriptional control of these immunoregulatory molecules.
- Cytokine expression and gene polymorphisms may serve as markers for severe Chagas disease susceptibility.
Conclusions:
- Immune responses and genetic factors play a critical role in Chagas disease progression.
- Understanding these mechanisms can lead to better disease management and control strategies.
- Cytokine and genetic markers show promise for identifying individuals at risk for severe Chagas disease.
Abstract:
Chagas disease, a neglected disease caused by the protozoan Trypanosoma cruzi, is endemic in 21 Latin American countries, affecting 6-8 million people. Increasing numbers of Chagas disease cases have also been reported in non-endemic countries due to migration, contamination via blood transfusions or organ transplantation, characterizing Chagas as an emerging disease in such regions. While most individuals in the chronic phase of Chagas disease remain in an asymptomatic clinical form named indeterminate, approximately 30% of the patients develop a cardiomyopathy that is amongst the deadliest cardiopathies known. The clinical distinctions between the indeterminate and the cardiac clinical forms are associated with different immune responses mediated by innate and adaptive cells. In this review, we present a collection of studies focusing on the human disease, discussing several aspects that demonstrate the association between chemokines, cytokines, and cytotoxic molecules with the distinct clinical outcomes of human infection with Trypanosoma cruzi. In addition, we discuss the role of gene polymorphisms in the transcriptional control of these immunoregulatory molecules. Finally, we discuss the potential application of cytokine expression and gene polymorphisms as markers of susceptibility to developing the severe form of Chagas disease, and as targets for disease control.
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