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

Higuchi, Maria de Lourdes; Lopes, E. A.; Saldanha, Luís Balthazar; Barretto, Antônio Carlos Pereira; Stolf, Noedir A. G; Bellotti, Giovanni; Pileggi, F

doi:10.1590/s0036-46651986000200004

Cited by 9 publications

(3 citation statements)

References 12 publications

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“…This interpretation was supported by the finding of autologous immunoglobulins and complement in the endothelia and sarcolemmas of heart biopsies from chagasic humans (4, 16). However, those findings have not been confirmed recently, and doubts were raised about the validity of these observations (7,11). Since studies were performed by immunohistochemical methods and with frozen myocardium as the target, the possibility exists that antigens are destroyed during processing.…”

Section: Discussionmentioning

confidence: 95%

Antiheart antibody-dependent cytotoxicity in the sera of mice chronically infected with Trypanosoma cruzi

1988

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Sera of mice chronically infected with Trypanosoma cruzi contain antibodies that bind to the surface of living adult syngeneic heart muscle cells. In a syngeneic system, with nonadherent spleen mononuclear cells as effector cells and cardiocytes as targets, antibody-dependent cytotoxicity (ADCC), revealed by the liberation of creatine phosphokinase from damaged cardiocytes, was observed after incorporation of serum samples from infected mice. Target damage was decreased after absorption with syngeneic myocardium, but absorption with T. cruzi epimastigotes or trypomastigotes or with syngeneic skeletal muscle had no effect on ADCC. No complement-dependent lysis against heart muscle cells was detected in the same serum samples. These observations indicate that serum from chronically chagasic mice contain antibodies that bind to the surface of living adult syngeneic cardiocytes and are able to exert ADCC, suggesting that they could play a role in the pathogenesis of the heart damage that occurs in Chagas' disease.

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Section: Discussionmentioning

confidence: 95%

Antiheart antibody-dependent cytotoxicity in the sera of mice chronically infected with Trypanosoma cruzi

1988

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“…Chagas cardiomyopathy is the most severe and life-threatening manifestation of human disease caused by the protozoan parasite Trypanosoma cruzi (Marin-Neto et al, 2007 ). The knowledge of pathological changes in Chagas heart disease is largely derived from necropsy studies and endomyocardial biopsy of humans and observations in several experimental models that reasonably reproduce the various stages of the disease (Higuchi Mde et al, 1986 ; de Souza et al, 2001 ). The clinical manifestations and the tissue damage itself are closely associated with parasite multiplication and the consequent immunological reaction triggered in the parasitized myocardium (Marin-Neto et al, 2007 ).…”

Section: Discussionmentioning

confidence: 99%

Circulating Plasma MicroRNA-208a as Potential Biomarker of Chronic Indeterminate Phase of Chagas Disease

et al. 2018

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Chagas cardiomyopathy is the most severe clinical manifestation of chronic Chagas disease. The disease affects most of the Latin American countries, being considered one of the leading causes of morbidity and death in the continent. The pathogenesis of Chagas cardiomyopathy is very complex, with mechanisms involving parasite-dependent cytopathy, immune-mediated myocardial damage and neurogenic disturbances. These pathological changes eventually result in cardiac myocyte hypertrophy, arrhythmias, congestive heart failure and stroke during chronic infection phase. Herein, we show that miR-208a, a microRNA that is a key factor in promoting cardiovascular dysfunction during cardiac hypertrophy processes of heart failure, has its circulating levels increased during chronic indeterminate phase when compared to cardiac (CARD) clinical forms in patients with Chagas disease. In contrast, we have not found altered serum levels of miR-34a, a microRNA known to promote pro-apoptotic role in myocardial infarction during degenerative process of cardiac injuries thus indicating intrinsic differences in the nature of the mechanisms underlying the heart failure triggered by Trypanosoma cruzi infection. Our findings support that the chronic indeterminate phase is a progressive phase involved in the genesis of chagasic cardiopathy and point out the use of plasma levels of miR-208a as candidate biomarker in risk-prediction score for the clinical prognosis of Chagas disease.

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“…The number of parasites in the cardiac tissue of CCC patients is scarce. This, together with the finding of immunoglobulins with affinity to muscarinic receptors and β-1 adrenergic expressed in the cardiomyocyte surface and the appearance of cytotoxic T lymphocytes with reactivity toward myocardial fibers, suggested that the etiology of CCC was autoimmune [53][54][55][56][57]. Investigations performed during the last 30 years in animal models infected with T. cruzi and patients with Chagas disease have modified this theory.…”

Section: Chagasic Chronic Cardiomyopathymentioning

confidence: 99%

Modulation of Host Cell Apoptosis byTrypanosoma cruzi: Repercussions in the Development of Chronic Chagasic Cardiomyopathy

Román-Carraro¹,

Coria-Paredes²,

Wilkins‐Rodríguez³

et al. 2022

Chagas Disease - From Cellular and Molecular Aspects of Trypanosoma Cruzi-Host Interactions to the Clinical Intervention

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Trypanosoma cruzi is an intracellular parasite, which causes Chagas disease, affecting millions of people throughout the world. T. cruzi can invade several cell types, among which macrophages and cardiomyocytes stand out. Chagas disease goes through two stages: acute and chronic. If it becomes chronic, its most severe form is the chagasic chronic cardiomyopathy, which accounts for most of the fatalities due to this disease. For parasites to persist for long enough in cells, they should evade several host immune responses, one of these being apoptosis. Apoptosis is a type of programmed cell death described as a well-ordered and silent collection of steps that inevitably lead cells to a noninflammatory death. Cells respond to infection by initiating their own death to combat the infection. As a result, several intracellular microorganisms have developed different strategies to overcome host cell apoptosis and persist inside cells. It has been shown that T. cruzi has the ability to inhibit host cells apoptosis and can also induce apoptosis of cells that combat the parasite such as cytotoxic T cells. The aim of this chapter is to present up-to-date information about the molecules and mechanisms engaged by T. cruzi to achieve this goal and how the modulation of apoptosis by T. cruzi reflects in the development of chronic chagasic cardiomyopathy.

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

Cited by 9 publications

References 12 publications

Antiheart antibody-dependent cytotoxicity in the sera of mice chronically infected with Trypanosoma cruzi

Antiheart antibody-dependent cytotoxicity in the sera of mice chronically infected with Trypanosoma cruzi

Circulating Plasma MicroRNA-208a as Potential Biomarker of Chronic Indeterminate Phase of Chagas Disease

Modulation of Host Cell Apoptosis byTrypanosoma cruzi: Repercussions in the Development of Chronic Chagasic Cardiomyopathy

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