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Measurement of Antibody Effects on Cellular Function of Isolated Cardiomyocytes
Published on: March 8, 2013
Immunohistochemical studies in acute and chronic canine chagasic cardiomyopathy
Marcelo V Caliari1, Marta de Lana, Rosângela A F Cajá
1Laboratorio de Patologia Comparada, Departamento de Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Pampulha, Belo Horizonte, Minas Gerais, Brazil CEP 31.270.901. caliari@icb.ufmg.br
Insights
Canine Chagas
Area of Science:
- Immunology
- Veterinary Pathology
- Infectious Diseases
Background:
- Chagas' disease in dogs is characterized by mononuclear cell myocarditis.
- The role of specific immune cell populations in canine chagasic myocarditis is not fully understood.
- Trypanosoma cruzi infection can lead to chronic inflammatory heart disease in canines.
Purpose of the Study:
- To quantify canine CD8(+) T cells, CD4(+) T cells, and neutrophils in experimental canine chagasic myocardiopathy.
- To evaluate the influence of tissue parasitism on the development of chronic myocarditis.
- To compare the immune response induced by two different Trypanosoma cruzi strains.
Main Methods:
- Monoclonal antibodies and image analysis were used to quantify immune cells.
- Immunohistochemistry was employed to detect parasite presence and host immune response.
- Canine models were infected with two distinct Trypanosoma cruzi strains (Berenice 78 and Berenice 62).
Main Results:
- A predominance of T lymphocytes was observed in the inflammatory infiltrate of affected dogs.
- The Berenice 78 strain induced a higher proliferation of CD8(+) T cells compared to CD4(+) T cells, especially during the acute phase.
- Chronic myocarditis induced by the Berenice 62 strain showed a T cell proportion similar to normal canine lymphoid organs.
- Parasite presence was not detected in the myocardium during the chronic phase, suggesting non-parasitic mechanisms in inflammation.
Conclusions:
- Canine CD8(+) T cells may play a significant role in the pathogenesis of Chagas' disease-induced myocarditis, particularly with the Berenice 78 strain.
- The absence of detectable parasites in chronic myocarditis indicates that immune-mediated mechanisms are crucial for sustained cardiac damage.
- Different Trypanosoma cruzi strains can elicit distinct immune responses and varying degrees of myocardial injury in dogs.
Abstract:
A major characteristic of Chagas' disease is a myocarditis constituted primarily of mononuclear cells, both during the acute and chronic phases of the disease. Using monoclonal antibodies and image analyses we have quantified canine CD8(+) T cells (caCD8(+) T cells), canine CD4(+) T cells (caCD4(+) T cells) and neutrophils in canine chagasic myocardiopathy induced by two strains isolated from the first human clinical case of Chagas' disease. We also evaluated the influence of tissue parasitism in the genesis of chronic myocarditis through immunohistochemistry. As in human myocarditis, there was a predominance of T lymphocytes in the inflammatory infiltrate in all animals studied. In the dogs inoculated with strain Berenice 78 (Be78) and necropsied during the acute phase of infection, we found 58% caCD8(+) and 42% caCD4(+) T cells. In chronically infected animals, 53% of T cells were represented by caCD8(+) and 47% were caCD4(+) T cells. Since normal canine lymphoid organs are constituted by 70-80% caCD4(+) T cells and 20-30% caCD8(+) T cells our results indicate a higher proliferation of caCD8(+) T cells in dogs inoculated with the Be78 strain. In chronic myocarditis induced by the Berenice 62 (Be62) strain, caCD8(+) cells constituted 33% of the T cells and 67% were caCD4(+) T cells, a proportion similar to that found in normal canine lymphoid organs. Since the Be78 strain induces greater loss of myocardiocytes than strain Be62, we believe that the caCD8(+) T cells, among other factors, can be important in the genesis of these lesions. Amastigote nests and immunohistochemically labelled Trypanosoma cruzi antigen were not found in dogs necropsied during the chronic phase. The absence of the parasite in the myocardium suggests the involvement of other mechanisms in the genesis of the inflammatory process.
