Differential tissue tropism of Trypanosoma cruzi strains: an in vitro study

Andrade, Luciana O.; Galvao, L. M. C.; Meirelles, Maria de Nazareth Leal de; Chiari, Égler; Pena, Sérgio D.J.; Macedo, Andréa Mara

doi:10.1590/s0074-02762010000600018

Cited by 46 publications

(56 citation statements)

References 21 publications

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“…This selection was due to higher intracellular multiplication of the JG strain (26). Another study conducted using a mixture of Tc I and Tc II strains in murine and human macrophages also showed that Tc II strains have a higher proliferative ability, as well as lower doubling time inside macrophages, as compared to Tc I (27).…”

Section: Chagas Disease: a Complex Host-parasite Interaction Drives Pmentioning

confidence: 99%

Immunoregulatory networks in human Chagas disease

Dutra

Menezes

Magalhães

et al. 2014

Parasite Immunology

136

133

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Summary Chagas disease, caused by the infection with Trypanosoma cruzi, is endemic in all Latin America. Due to the increase in population migration, Chagas disease has spread worldwide and is now considered a health issue not only in endemic countries. While most chronically infected individuals remain asymptomatic, approximately 30% of the patients develop a potentially deadly cardiomyopathy. The exact mechanisms that underlie the establishment and maintenance of the cardiac pathology are not clear. However, there is consistent evidence that immunoregulatory cytokines are critical for orchestrating the immune response and, thus, influence disease development or control. While the asymptomatic (indeterminate) form represents a state of balance between the host and the parasite, the establishment of the cardiac form represents the loss of this balance. Analysis of data obtained from several studies have led to the hypothesis that the indeterminate form is associated with an anti-inflammatory cytokine profile, represented by high expression of IL-10, while cardiac form is associated with a high production of IFN-gamma and TNF-alpha in relation to IL-10, leading to an inflammatory profile. Here, we discuss the immunoregulatory events that might influence disease outcome, as well as the mechanisms that influence the establishment of these complex immunoregulatory networks.

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Section: Chagas Disease: a Complex Host-parasite Interaction Drives Pmentioning

confidence: 99%

Immunoregulatory networks in human Chagas disease

Dutra

Menezes

Magalhães

et al. 2014

Parasite Immunology

136

133

View full text Add to dashboard Cite

show abstract

“…Although infective T. cruzi trypomastigotes are capable of invading a wide variety of tissues and cell types in the vertebrate host, the majority of T.cruzi laboratory strains and isolates have tropism for cardiac tissue and or cardiomyocytes [32] . The establishment of a long-term infection in the heart and the development of a cardiomyopathy condition are directly related to the ability of T. cruzi to infect and persist within cardiomyocytes during the acute phase of infection [33,34] .…”

Section: Tcruzimentioning

confidence: 99%

Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy

Ferreira¹,

Frade²,

Baron³

et al. 2014

WJC

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Chagas disease cardiomyopathy (CCC), the main consequence of Trypanosoma cruzi (T.cruzi ) infection, is an inflammatory cardiomyopathy that develops in up to 30% of infected individuals. The heart inflammation in CCC patients is characterized by a Th1 T cell-rich myocarditis with increased production of interferon (IFN)-γ, produced by the CCC myocardial infiltrate and detected at high levels in the periphery. IFN-γ has a central role in the cardiomyocyte signaling during both acute and chronic phases of T.cruzi infection. In this review, we have chosen to focus in its pleiotropic mode of action during CCC, which may ultimately be the strongest driver towards pathological remodeling and heart failure. We describe here the antiparasitic protective and pathogenic dual role of IFN-γ in Chagas disease.

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“…Patients infected with T. cruzi I demonstrated a higher prevalence of cardiac alterations than those infected with T. cruzi II (Ramírez et al, 2010). These two DTUs behave differently with respect to their virulence, capacity for cell invasion, infectiveness (reviewed by Mortara et al, 2005;Andrade et al, 2010), capacity for vector transmission (Lana et al, 1998), and resistance to chemotherapeutic agents .…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzi I–III in southern Brazil causing individual and mixed infections in humans, sylvatic reservoirs and triatomines

et al. 2011

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The aim of this study was to characterise Discrete Typing Units (DTUs) of 28 isolates of Trypanosoma cruzi from humans (15), triatomines (9), and opossums (4) in the state of Paraná, southern Brazil. For this purpose, we analysed the size polymorphism at the 3' end of the 24Sα ribosomal RNA gene (rRNA) and the restriction fragment length polymorphism (RFLP) of the partial 5' sequence of the mitochondrial Cytochrome Oxidase subunit II gene (COII). Band patterns of the isolates were compared with reference samples of T. cruzi I (Silvio X10 and Col 17G2), T. cruzi II (Esmeraldo and JG), T. cruzi III (222 and 231), T. cruzi IV (CAN III), T. cruzi V (SO3 cl5), and T. cruzi VI (CL Brener). Our results confirmed that rRNA analysis is of limited use for assessing T. cruzi DTUs. COII RFLP analysis was suitable for screening, but for one isolate it was necessary to determine the COII partial sequence to identify the DTU. Only one of the isolates from humans belonged to T. cruzi I; 13 isolates belonged to T. cruzi II and one to T. cruzi III. The four isolates from opossums and five isolates from triatomines were identified as T. cruzi I. Four isolates from triatomines showed patterns of both T. cruzi I and II, indicating mixed infections. This study contributes to the characterisation of the dynamics of T. cruzi populations in southern Brazil.

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Differential tissue tropism of Trypanosoma cruzi strains: an in vitro study

Cited by 46 publications

References 21 publications

Immunoregulatory networks in human Chagas disease

Immunoregulatory networks in human Chagas disease

Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy

Trypanosoma cruzi I–III in southern Brazil causing individual and mixed infections in humans, sylvatic reservoirs and triatomines

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