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Published on: May 26, 2021
Bone marrow cell migration to the heart in a chimeric mouse model of acute chagasic disease
Camila Iansen Irion1, Bruno Diaz Paredes1, Guilherme Visconde Brasil1
1Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.
Insights
Chagas disease research shows bone marrow cells do not migrate to the heart in infected chimeric mice, despite observed cardiac dysfunction. This study investigates Trypanosoma cruzi infection effects on bone marrow cell migration.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- Chagas disease, caused by Trypanosoma cruzi, is a significant public health concern with no effective treatments.
- The role of bone marrow-derived cells in Chagas disease, particularly their cardiac effects and migration patterns, remains poorly understood.
- Studies on chimeric mouse models for chagasic cardiomyopathy are limited, hindering mechanistic insights.
Purpose of the Study:
- To investigate the migration of bone marrow cells to the heart following Trypanosoma cruzi infection.
- To utilize a chimeric mouse model to study Chagas disease pathogenesis.
- To explore potential therapeutic targets by understanding cell dynamics in the infected heart.
Main Methods:
- Chimeric mice were generated by irradiating wild-type C57BL6 mice and infusing them with bone marrow cells from green fluorescent protein (GFP)-transgenic mice.
- Experimental groups included infected chimeric (iChim), infected wild-type (iWT), non-infected chimeric (Chim), and non-infected wild-type (WT) mice.
- Mice were infected with Trypanosoma cruzi (Brazil strain), and cardiac function and cell populations were assessed one month post-infection.
Main Results:
- Infected chimeric and wild-type mice exhibited first-degree atrioventricular block, reduced heart rate, and impaired exercise capacity compared to non-infected controls.
- iChim mice showed increased parasitemia, myocarditis, and amastigote nests in heart tissue compared to iWT mice.
- Flow cytometry did not detect hematopoietic progenitor cells or GFP+ cardiomyocytes in the hearts of infected chimeric mice.
Conclusions:
- Bone marrow cell migration to the heart was not detected in this chimeric mouse model of Chagas disease.
- Despite cardiac dysfunction, hematopoietic progenitor cells and derived cardiomyocytes were not found in the infected hearts.
- Further research is needed to elucidate the mechanisms of bone marrow cell influence, if any, in chagasic cardiomyopathy.
Background:
Chagas disease is a public health problem caused by infection with the protozoan Trypanosoma cruzi. There is currently no effective therapy for Chagas disease. Although there is some evidence for the beneficial effect of bone marrow-derived cells in chagasic disease, the mechanisms underlying their effects in the heart are unknown. Reports have suggested that bone marrow cells are recruited to the chagasic heart; however, studies using chimeric mouse models of chagasic cardiomyopathy are rare.
Objectives:
The aim of this study was to investigate the migration of bone marrow cells to the heart after T. cruzi infection in a model of chagasic disease in chimeric mice.
Methods:
To obtain chimerical mice, wild-type (WT) C57BL6 mice were exposed to full body irradiation (7 Gy), causing bone marrow ablation. Then, bone marrow cells from green fluorescent protein (GFP)-transgenic mice were infused into the mice. Graft effectiveness was confirmed by flow cytometry. Experimental mice were divided into four groups: (i) infected chimeric (iChim) mice; (ii) infected WT (iWT) mice, both of which received 3 × 104 trypomastigotes of the Brazil strain; (iii) non-infected chimeric (Chim) mice; and (iv) non-infected WT mice.
Findings:
At one-month post-infection, iChim and iWT mice showed first degree atrioventricular block with decreased heart rate and treadmill exercise parameters compared to those in the non-infected groups.
Main Conclusions:
iChim mice showed an increase in parasitaemia, myocarditis, and the presence of amastigote nests in the heart tissue compared to iWT mice. Flow cytometry analysis did not detect haematopoietic progenitor cells in the hearts of infected mice. Furthermore, GFP+ cardiomyocytes were not detected in the tissues of chimeric mice.
