Protein deficiency alters CX3CL1 and endothelin-1 in experimental Trypanosoma cruzi-induced cardiomyopathy
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Updated: May 14, 2026

Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
Published on: July 29, 2012
Régia F Martins1, Patrícia M Martinelli, Paulo M M Guedes
1Núcleo de Pesquisas em Ciências Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, Brazil.
Insights
Protein malnutrition exacerbates Chagas heart disease by increasing endothelin-1 and CX3CL1 levels. This nutritional deficiency impairs the host
Area of Science:
- Immunology
- Nutritional Science
- Parasitology
Background:
- Chagas heart disease, a complication of Trypanosoma cruzi infection, is influenced by host nutritional status.
- Protein malnutrition can lead to secondary immunodeficiency, potentially worsening parasitic infections.
- Endothelin-1 and CX3CL1 are implicated in inflammatory processes.
Purpose of the Study:
- To investigate the impact of a low protein diet on endothelin-1 and CX3CL1 production in a Trypanosoma cruzi infection model.
- To assess the role of nutritional status in modulating inflammatory mediators during Chagas disease.
Main Methods:
- Fisher rats were fed either a low protein (6%) or normal protein (15%) diet.
- Animals were infected with the Y strain of Trypanosoma cruzi.
- Parasitemia, immune cell infiltration (including macrophage phenotypes), and levels of endothelin-1 and CX3CL1 were evaluated at acute and chronic phases.
Main Results:
- Low protein diet reduced body weight and serum proteins but elevated circulating CX3CL1 and endothelin-1 in infected rats.
- Infected rats on a low protein diet showed uncontrolled parasitemia.
- Cardiac tissue in the acute phase exhibited reduced CX3CL1, endothelin-1, and leukocyte infiltration, particularly CD68 and CD163 macrophages, in the low protein group.
Conclusions:
- Endothelin-1 and CX3CL1 play a role in the inflammatory response during Chagas disease.
- Host nutritional status, specifically protein intake, can modulate the levels of these inflammatory mediators.
- Dietary protein influences the control of parasitemia and cardiac inflammation in experimental Chagas disease.
Objective:
Chagas heart disease is developed as a result of the infection with Trypanosoma cruzi. Protein malnutrition contributes to secondary immunodeficiency. The aim of this study was to investigate the role of a low protein diet on the production of endothelin-1 and CX3CL1 in blood and cardiac tissue samples in an experimental model with T. cruzi infection.
Methods:
Fisher rats were submitted to low protein (6%) and normal protein (15%) diets and then infected with the Y strain of T. cruzi. At days 15 and 120, parasites and immune cells were evaluated.
Results:
The low protein diet reduced body weight and circulating serum proteins, but promoted elevation of CX3CL1 and endothelin-1 levels in infected animals, which were unable to control blood parasitemia replication. In heart tissue, the low protein diet reduced cardiac CX3CL1, endothelin-1 and leucocyte infiltration in the acute phase, in particular CD68 and CD163 macrophage phenotypes.
Conclusion:
Together, these results highlight the participation of endothelin-1 and CX3CL1 in the inflammatory process of Chagas diesease, both being mediators partially controlled by the host nutritional status.
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