Infection-Associated Vasculopathy in Experimental Chagas Disease

Scharfstein, Júlio; Andrade, Daniele

doi:10.1016/b978-0-12-385895-5.00005-0

Cited by 19 publications

(18 citation statements)

References 111 publications

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“…suggesting that proinflammatory phenotypes of T. cruzi strains may be ascribed, at least in part, to variable expression of TLR2 ligands and cruzipain isoforms during the acute myocarditis (Scharfstein and Andrade, 2011). However, a detailed understanding of the contribution of host and parasite genetics in this process is lacking.…”

Section: Discusionmentioning

confidence: 99%

Trypanosoma cruzi strains cause different myocarditis patterns in infected mice

et al. 2014

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Esta es la versión de autor del artículo publicado en: This is an author produced version of a paper published in:Acta Tropica 139 (2014) pancarditis with inflammatory infiltrates along the epicardium, whereas Sc43 caused inflammation preferentially in the auricles in association with intracellular parasite localization. We observed intramyocardic perivasculitis in mice infected with the VFRA and Y strains, but not with Sc43, during the acute phase, which suggests that endothelial cells may be involved in heart colonization by these more virulent strains. In in vitro infection assays, the Y strain had the highest parasite-cell ratio in epithelial, macrophage and endothelial cell lines, but Y and VFRA strains were higher than Sc43 in cardiomyocytes. Conclusions. This study supports parasite variability as a cause for the diverse cardiac outcomes observed in Chagas disease, and suggests that endothelial cells could be involved in heart infection during the acute phase.3

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Section: Discusionmentioning

confidence: 99%

Trypanosoma cruzi strains cause different myocarditis patterns in infected mice

et al. 2014

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“…Similar alterations have been found in other models of experimental T. cruzi infection, including the development of typical ventricular aneurysms 24 . The mechanisms responsible for occlusive platelet thrombosis and microcirculatory spasm were directly related to the T. cruzi infection causing endothelial cell damage 25 and indirectly related to the interaction of the endothelium with immune effector cells 26,27 . In vitro studies of T. cruzi infection of human umbilical vein endothelium cells showed increased production of endothelin.…”

Section: Evidence From Animal Models Of T Cruzi Infection and In Vitmentioning

confidence: 99%

Pathogenesis of chronic Chagas cardiomyopathy: the role of coronary microvascular derangements

Marin-Neto

Simões

Rassi

2013

Rev. Soc. Bras. Med. Trop.

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There is ample experimental and clinical evidence of functional and structural microvascular abnormalities occurring in patients with Chagas cardiomyopathy, possibly due to the infl ammatory process and/or autonomic disturbances caused by Trypanosoma cruzi infection. Those microvascular derangements are likely to constitute at least an ancillary factor that potentiates and amplifi es the chronic infl ammation in myocardial tissue. It is possible to devise appropriate therapeutic interventions aimed at reverting or slowing the progression of the microvascular abnormalities to positively affect the natural history of Chagas cardiomyopathy.

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“…Clinically, T. cruzi infection causes acute myocarditis, followed by chronic cardiomyopathy, in humans and experimental models (Scharfstein and Andrade, 2011; Henao-Martínez et al, 2015). Most infected individuals remain asymptomatic for several years.…”

Section: Introductionmentioning

confidence: 99%

Moderate Treadmill Exercise Training Improves Cardiovascular and Nitrergic Response and Resistance to Trypanosoma cruzi Infection in Mice

et al. 2017

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There is evidence suggesting that exercise training (ET) acts as a factor toward resistance to Trypanosoma cruzi infection. However, the effects of mean arterial pressure (MAP), heart rate (HR), and nitric oxide (NO) during the acute phase of infection has not been elucidated yet. Swiss mice were randomly assigned into four groups: sedentary control (SC, n = 30), trained control (TC, n = 30), sedentary infected (SI, n = 30), and trained infected (TI, n = 30). ET was performed on the treadmill for 9 weeks. After training, the mice were infected with 5 × 103 trypomastigotes of T. cruzi (Y strain) or PBS. We observed resting bradycardia and improved performance in trained animals compared with sedentary ones. On the 20th day post-infection (DPI), we found a decrease in HR in SI animals compared to TI animals (699.73 ± 42.37 vs. 742.11 ± 25.35 bpm, respectively, P < 0.05). We also observed increased production of NO in cardiac tissue on the 20th DPI in the SI group, normalized in TI group (20.73 ± 2.74 vs. 6.51 ± 1.19 μM, respectively). Plasma pro-inflammatory cytokines (IL-12, TNF-α, IFN-γ,) and MCP-1 were increased in SI animals, but decreased in TI animals. The increase in parasitemia on the 15th and 17th DPI in the SI group was attenuated in the TI group. Our results suggest that previous ET plays a preventive role in resistance to T. cruzi infection, modulating cardiovascular aspects, inflammatory reaction, and NO levels of infected mice.

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Infection-Associated Vasculopathy in Experimental Chagas Disease

Cited by 19 publications

References 111 publications

Trypanosoma cruzi strains cause different myocarditis patterns in infected mice

Trypanosoma cruzi strains cause different myocarditis patterns in infected mice

Pathogenesis of chronic Chagas cardiomyopathy: the role of coronary microvascular derangements

Moderate Treadmill Exercise Training Improves Cardiovascular and Nitrergic Response and Resistance to Trypanosoma cruzi Infection in Mice

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