Chagas heart disease: Report on recent developments

Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Cardiology in review (Impact Factor: 2.41). 03/2012; 20(2):53-65. DOI: 10.1097/CRD.0b013e31823efde2
Source: PubMed


Chagas disease, caused by the parasite Trypanosoma cruzi, is an important cause of cardiac disease in endemic areas of Latin America. It is now being diagnosed in nonendemic areas because of immigration. Typical cardiac manifestations of Chagas disease include dilated cardiomyopathy, congestive heart failure, arrhythmias, cardioembolism, and stroke. Clinical and laboratory-based research to define the pathology resulting from T. cruzi infection has shed light on many of the cellular and molecular mechanisms leading to these manifestations. Antiparasitic treatment may not be appropriate for patients with advanced cardiac disease. Clinical management of Chagas heart disease is similar to that used for cardiomyopathies caused by other processes. Cardiac transplantation has been successfully performed in a small number of patients with Chagas heart disease.

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Available from: Linda A Jelicks, Oct 02, 2015
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    • "The multitude of invasive strategies employed by T. cruzi varies widely between strains and isolates and represents an important obstacle in the development of suitable chemotherapy. T. cruzi has several life cycle stages namely: bloodstream and metacyclic trypomastigotes , which do not replicate but infect mammalian cells; amastigotes, which replicate within host cells; and epimastigotes , which are found in insects and replicate extracellularly , but do not infect host cells [2]. It has recently been appreciated that there are both intracellular and extracellular amastigotes. "
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    ABSTRACT: Trogocytosis was originally thought to be restricted to the interaction of cells of the immune system with cancer cells. Such membrane exchanges are probably a general process in cell biology, and membrane exchange has been demonstrated to occur between non-immune cells within an organism. Herein, we report that membrane and protein exchange, consistent with trogocytosis, between Trypanosoma cruzi (both the Brazil and Tulahuen strains) and the mammalian cells it infects. Transfer of labeled membrane patches was monitored by labeling of either parasites or host cells, i.e. human foreskin fibroblasts and rat myoblasts. Trypomastigotes and amastigotes transferred specific surface glycoproteins to the host cells along with membranes. Exchange of membranes between the parasite and host cells occurred during successful invasion. Extracellular amastigotes did not transfer membrane patches and were did not transfer either membranes or proteins to the host cells. Membrane exchange was also found to occur between interacting epimastigotes in cell-free culture and may be important in parasite-parasite interactions as well. Further studies should provide new insights into pathogenesis and provide targets for therapeutic intervention. Copyright © 2014 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
    Microbes and Infection 11/2014; 17(1). DOI:10.1016/j.micinf.2014.10.009 · 2.86 Impact Factor
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    • "The protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease, which affects approximately 15 million people in South and Central America [1] [2]. It is estimated that about 30% of infected individuals will develop severe chronic forms of the disease, especially the often fatal Chagas disease cardiomyopathy (CCC) [1] [2] [3] [4]. Intracellular protozoan parasites are potent stimulators of innate and cell-mediated immunity. "
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    ABSTRACT: Chagas disease, caused by the protozoan parasite Trypanosoma cruzi (T. cruzi), is characterized by immunopathology driven by IFN-γ secreting Th1-like T cells. T. cruzi has a thick coat of mucin-like glycoproteins covering its surface, which plays an important role in parasite invasion and host immunomodulation. It has been extensively described that T. cruzi or its products-like GPI anchors isolated from GPI-anchored mucins from the trypomastigote life cycle stage (tGPI-mucins)-are potent inducers of proinflammatory responses (i.e., cytokines and NO production) by IFN-γ primed murine macrophages. However, little is known about whether T. cruzi or GPI-mucins exert a similar action in human cells. We therefore decided to further investigate the in vitro cytokine production profile from human mononuclear cells from uninfected donors exposed to T. cruzi as well as tGPI-mucins. We observed that both living T. cruzi trypomastigotes and tGPI-mucins are potent inducers of IL-12 by human peripheral blood monocytes and this effect depends on CD40-CD40L interaction and IFN-γ. Our findings suggest that the polarized T1-type cytokine profile seen in T. cruzi infected patients might be a long-term effect of IL-12 production induced by lifelong exposure to T. cruzi tGPI-mucins.
    Mediators of Inflammation 07/2014; 2014:345659. DOI:10.1155/2014/345659 · 3.24 Impact Factor
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    • "Chagas disease, a neglected tropical disease caused by the protozoan parasite Trypanosoma cruzi, is considered to be a public health problem [1], [2]. Over 10 million people are infected in Latin America and more than 100 million individuals live at risk of infection by blood transfusion, congenital, or oral transmission [3]. "
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    ABSTRACT: Trypanosoma cruzi, the causative agent of Chagas disease, is extremely resistant to ionizing radiation, enduring up to 1.5 kGy of gamma rays. Ionizing radiation can damage the DNA molecule both directly, resulting in double-strand breaks, and indirectly, as a consequence of reactive oxygen species production. After a dose of 500 Gy of gamma rays, the parasite genome is fragmented, but the chromosomal bands are restored within 48 hours. Under such conditions, cell growth arrests for up to 120 hours and the parasites resume normal growth after this period. To better understand the parasite response to ionizing radiation, we analyzed the proteome of irradiated (4, 24, and 96 hours after irradiation) and non-irradiated T. cruzi using two-dimensional differential gel electrophoresis followed by mass spectrometry for protein identification. A total of 543 spots were found to be differentially expressed, from which 215 were identified. These identified protein spots represent different isoforms of only 53 proteins. We observed a tendency for overexpression of proteins with molecular weights below predicted, indicating that these may be processed, yielding shorter polypeptides. The presence of shorter protein isoforms after irradiation suggests the occurrence of post-translational modifications and/or processing in response to gamma radiation stress. Our results also indicate that active translation is essential for the recovery of parasites from ionizing radiation damage. This study therefore reveals the peculiar response of T. cruzi to ionizing radiation, raising questions about how this organism can change its protein expression to survive such a harmful stress.
    PLoS ONE 05/2014; 9(5):e97526. DOI:10.1371/journal.pone.0097526 · 3.23 Impact Factor
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