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Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
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The Characterization of Cardiac Explants Reveals Unique Fibrosis Patterns and a Predominance of CD8+ T Cell
Martha Lucía Díaz1, Fredy A Delgado1, Ruth A Martínez1
1Immunology and Molecular Epidemiology Group, School of Microbiology, Universidad Industrial de Santander, Bucaramanga 680002, Colombia.
Insights
Chagas cardiomyopathy (CCC) shows unique myocardial changes, including extensive fibrosis and inflammation, with more memory T cells compared to other heart failure types. This suggests a critical role for parasite-specific immune responses in CCC progression.
Area of Science:
- Cardiology
- Immunology
- Pathology
Background:
- Chagas cardiomyopathy (CCC) is a significant cause of heart failure.
- Understanding the distinct pathological features of CCC is crucial for effective treatment.
- Comparing CCC to non-Chagas cardiomyopathies (NCC) can elucidate unique disease mechanisms.
Purpose of the Study:
- To histopathologically characterize myocardial tissue in end-stage heart failure (ESHF) patients with CCC versus NCC.
- To compare the phenotypes of inflammatory cells within the myocardial tissue of these patient groups.
- To identify differences in fibrosis and cellular infiltration between CCC and NCC.
Main Methods:
- Analysis of 32 explanted hearts from heart transplant recipients (21 CCC, 11 NCC).
- Macroscopic and microscopic examination of myocardial tissue.
- Flow cytometry to characterize inflammatory cell phenotypes, focusing on T cell subsets.
Main Results:
- CCC hearts exhibited more extensive fibrosis, collagen deposits, and cardiomyocyte degeneration than NCC hearts.
- Greater inflammatory infiltrates were observed in CCC.
- CCC hearts showed a higher proportion of memory T cells (CD8+CD45RO+) and fewer transitioning T cells (CD45RA+/CD45RO+) compared to NCC.
Conclusions:
- Chagas cardiomyopathy presents a distinct myocardial pathology with significant inflammation, fibrosis, and cardiomyocyte damage.
- The interplay between fibrosis and inflammatory cells in CCC suggests new research avenues for understanding disease progression.
- A predominance of memory T cells in CCC highlights the importance of the parasite-specific immune response in the disease course.
Aim:
The present study aimed to characterize the histopathological findings and the phenotype of inflammatory cells in the myocardial tissue of patients with end-stage heart failure (ESHF) secondary to CCC in comparison with ESHF secondary to non-Chagas cardiomyopathies (NCC).
Methods:
A total of 32 explanted hearts were collected from transplanted patients between 2014 and 2017. Of these, 21 were classified as CCC and 11 as other NCC. A macroscopic analysis followed by a microscopic analysis were performed. Finally, the phenotypes of the inflammatory infiltrates were characterized using flow cytometry.
Results:
Microscopic analysis revealed more extensive fibrotic involvement in patients with CCC, with more frequent foci of fibrosis, collagen deposits, and degeneration of myocardial fibers, in addition to identifying foci of inflammatory infiltrate of greater magnitude. Finally, cell phenotyping identified more memory T cells, mainly CD8+CD45RO+ T cells, and fewer transitioning T cells (CD45RA+/CD45RO+) in patients with CCC compared with the NCC group.
Conclusions:
CCC represents a unique form of myocardial involvement characterized by abundant inflammatory infiltrates, severe interstitial fibrosis, extensive collagen deposits, and marked cardiomyocyte degeneration. The structural myocardial changes observed in late-stage Chagas cardiomyopathy appear to be closely related to the presence of cardiac fibrosis and the colocalization of collagen fibers and inflammatory cells, a finding that serves as a basis for the generation of new hypotheses aimed at better understanding the role of inflammation and fibrogenesis in the progression of CCC. Finally, the predominance of memory T cells in CCC compared with NCC hearts highlights the critical role of the parasite-specific lymphocytic response in the course of the infection.
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