The TcI and TcII Trypanosoma cruzi experimental infections induce distinct immune responses and cardiac fibrosis in dogs

Trypanosoma cruzi infection may be caused by different strains with distinct discrete typing units (DTUs) that can result in variable clinical forms of chronic Chagas disease. The present study evaluates the immune response and cardiac lesions in dogs experimentally infected with different T. cruzi strains with distinct DTUs, namely, the Colombian (Col) and Y strains of TcI and TcII DTU, respectively. During infection with the Col strain, increased levels of alanine aminotransferase, erythrocytes, haematocrit and haemoglobin were observed. In addition, CD8+ T-lymphocytes isolated from the peripheral blood produced higher levels of interleukin (IL)-4. The latter suggests that during the acute phase, infection with the Col strain may remain unnoticed by circulating mononuclear cells. In the chronic phase, a significant increase in the number of inflammatory cells was detected in the right atrium. Conversely, infection with the Y strain led to leucopoenia, thrombopoenia, inversion of the ratio of CD4+/CD8+ T-lymphocytes and alterations in monocyte number. The Y strain stimulated the production of interferon-γ by CD4+ and CD8+ T-lymphocytes and IL-4 by CD8+ T-cells. In the chronic phase, significant heart inflammation and fibrosis were observed, demonstrating that strains of different DTUs interact differently with the host.

Immunocytochemical reaction of sera from chagasic patients against trypanosoma cruzi, intestine of triatoma infestans and normal human heart

Chagas disease has been considered by some authors as an autoimmune pathology and denied by others. In this paper we present by means of immunocytochemical reactions with sera of chagasic patients, evidence in favor of the presence of similar antigens in the parasite, vector and non chagasic human heart. The immunocytochemical technique used permits the localization by electron microscopy of the antigens in the peritrophic membrane of the parasite and basement membranes of the vectorïs midgut and of the myosin band of the normal human heart. These observations support the assumption of an autoimmune response in Chagas disease.

Autoimmunity in Chagas' heart disease

The time scale dissociation between high parasitemia and tissue pathology allied to the absence of parasites in the heart lesions of chronic Chagas' disease cardiopathy, casted doubt on the direct participation of Trypanosoma cruzi in tissue lesions. Moreover, the heart tissue lesions in chronic Chagas' disease cardiopathy are associated to an inflammatory mononuclear cell infiltrate, presumably the ultimate effectors of tissue damage. It has been hypothesized that the inflammatory cell infiltrate could mediate a delayed hypersensitivity process directed to the heart tissue components, an autoimmune response triggered by immunological cross-reactivity in the course of a protective immune response against some T. cruzi antigen homologous to heart proteins. However, little is known about the efector role of the T cells in the infiltrate, or about the nature of the antigen that lead to their accumulation in tissue. In this paper, we will review the published evidence on autoimmunity and immunological cross-reactivity between T cruzi and the mammalian host, along with data generated in our laboratory. The definition of the precise role played by autoimmunity in the pathogenesis of Chagas' disease cardiopathy may have important consequences both for immunoprophylaxis and for the therapeutic approach of chronic Chagas' disease.

Immunopathologic studies in myocardial biopsies of patients with Chagas' disease and idiopathic cardiomyopathy

Foram estudadas biópsias de ventrículo direito de 30 pacientes, 15 com doença crônica de Chagas e 15 com miocardiopatia congestiva idiopática. Analisou-se também cinco fragmentos miocárdicos obtidos de pacientes chagásicos com menos de duas horas de óbito. Os autores tentaram estabelecer, por meio de técnica de imunofluorescência direta, a presença de imunoglobulina G, A, e M, fibrinogênio e C3. Somente uma das 30 biópsias exibiu reaçäo positiva para IgG que era de um paciente com miocardiopatia congestiva idiopática. Todos os fragmentos provenientes de pacientes chagásicos näo apresentaram qualquer fluorescência com nenhum dos conjugados

Determinaçäo do anticorpo EVI na cardiopatia chagásica crônica / Determination of EVI antibodies in chronic Chagas' cardiopathy

Anticorpos EVI foram pesquisados no soro de 25 portadores de cardiopatia chagásica acompanhados no ambulatório e em 58 pessoas provenientes de área endêmica, a maioria delas sem sintomas. Anticorpo EVI foi encontrado em 93,10% de pacientes com doença cardíaca e em 96,61% dos demais, quando se utilizou coraçäo heterólogo como substrato, entretanto, nenhum caso foi positivo quando se utilizou tecido homólogo. O papel dos anticorpos EVI na doença de Chagas ainda näo está esclarecido, embora o presente trabalho sugeriu ser um epifenômeno decorrente da desmodulaçäo da resposta imune pela infecçäo crônica