Related Experiment Video
Updated: Oct 9, 2025
Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
Published on: June 23, 2022
Insights into CX3CL1/Fractalkine during experimental Trypanosoma cruzi infection
Tatiana Prata Menezes1, Bianca Alves Almeida Machado2, Débora Nonato Miranda Toledo1
1Laboratório de Imunobiologia da InflamaÇão/DECBI/ICEB, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brazil; Programa de PÓs-Graduação em Saúde e Nutrição, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brazil.
Insights
Trypanosoma cruzi infection increases inflammatory mediators like CX3CL1, TNF, and endothelin-1 in rats. CX3CL1 correlates with these factors, suggesting its role in Chagas disease myocarditis development.
Area of Science:
- Immunology
- Parasitology
- Cardiovascular Research
Background:
- Trypanosoma cruzi infection causes progressive myocarditis in mammals.
- The chemokine CX3CL1 may play a role in controlling parasite load during infection.
Purpose of the Study:
- To investigate the systemic and cardiac release of CX3CL1 during experimental T. cruzi infection.
- To determine the correlation between CX3CL1, endothelin-1, and TNF in T. cruzi-infected rats.
Main Methods:
- Male Fisher rats were infected with T. cruzi.
- Parasitemia was monitored daily.
- Immunoassays were performed on serum and cardiac tissue to measure CX3CL1, endothelin-1, and TNF levels on days 5 and 15 post-infection.
Main Results:
- T. cruzi infection significantly increased serum and cardiac levels of CX3CL1, endothelin-1, and TNF.
- CX3CL1 showed a positive correlation with TNF and endothelin-1 on both days 5 and 15 of infection.
Conclusions:
- CX3CL1 is involved in the inflammatory response during T. cruzi infection.
- The findings reinforce CX3CL1's participation in the development of T. cruzi-induced myocarditis.
Abstract:
Trypanosoma cruzi triggers a progressive myocarditis in mammalians through activation and recruitment of leukocytes and release of inflammatory mediators. The chemokine CX3CL1 has been highlighted for its potential role in the parasite controlling in end-pathological status of infected hosts. This study investigated the systemic and cardiac release of CX3CL1 in experimental T. cruzi infection and how this chemokine correlates with endothelin-1 and TNF. Male Fisher rats (n = 20) were infected, or not, by the Y strain of T. cruzi and parasitemia was daily evaluated and immunoassays performed in the cardiac tissue macerated supernatant and in serum to evaluate CX3CL1, endothelin, and TNF production on days 5 and 15 of infection. T. cruzi infection induced a higher serum and cardiac production of these mediators on days 5 and 15 of infection. In both periods of infection, respectively, CX3CL1 showed a positive correlation with TNF (r = 0.833, p < 0.001 and r = 0.723, p < 0.001) and endothelin-1 (r = 0.801, p < 0.05 and r = 0.857, p < 0.001), which reinforce its participation in the T. cruzi-induced myocarditis development.
