Neurodegeneration and Neuroregeneration in Chagas Disease

Chuenkova, Marina V.; PereiraPerrin, Mercio

doi:10.1016/b978-0-12-385895-5.00009-8

Cited by 30 publications

(18 citation statements)

References 226 publications

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“…These mimetics likely help maintain a balance between tissue damage and repair and contribute to the absence of cardiac and gastrointestinal abnormalities and survival of patients with acute Chagas disease and the majority of patients who stay in the indeterminate phase for prolonged periods of time (Rassi et al ., 2010). This hypothesis is consistent with the observations of neuronal loss in chagasic heart and the gastrointestinal tract, which occurs predominantly during the acute infection and remains at a steady state in the indeterminate phase (Chuenkova and Pereiraperrin, 2011). Autonomic dysfunction due to decreased innervations can be detected in patients with the indeterminate form of the disease, the patients are nevertheless asymptomatic and without pathology as indicated by electrocardiogram and radiological examinations.…”

Section: Parasite‐derived Cell Protective Mechanismssupporting

confidence: 92%

Mechanisms of Trypanosoma cruzi persistence in Chagas disease

Nagajyothi¹,

Machado

Burleigh

et al. 2012

Cellular Microbiology

142

107

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Summary Trypanosoma cruzi infection leads to development of chronic Chagas disease. In this article, we provide an update on the current knowledge of the mechanisms employed by the parasite to gain entry into the host cells and establish persistent infection despite activation of a potent immune response by the host. Recent studies point to a number of T. cruzi molecules that interact with host cell receptors to promote parasite invasion of the diverse host cells. T. cruzi expresses an antioxidant system and thromboxane A2 to evade phagosomal oxidative assault and suppress the host’s ability to clear parasites. Additional studies suggest that besides cardiac and smooth muscle cells that are the major target of T. cruzi infection, adipocytes and adipose tissue serve as reservoirs from where T. cruzi can recrudesce and cause disease decades later. Further, T. cruzi employs at least four strategies to maintain a symbiotic-like relationship with the host, and ensure consistent supply of nutrients for its own survival and long-term persistence. Ongoing and future research will continue to help refining the models of T. cruzi invasion and persistence in diverse tissues and organs in the host.

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Section: Parasite‐derived Cell Protective Mechanismssupporting

confidence: 92%

Mechanisms of Trypanosoma cruzi persistence in Chagas disease

Nagajyothi¹,

Machado

Burleigh

et al. 2012

Cellular Microbiology

142

107

View full text Add to dashboard Cite

show abstract

“…In the thymus, in particular, TS triggers apoptosis of immature CD4 + CD8 + thymocytes inside the nurse cell complexes [73, 74], which may lead to the transient thymic aplasia observed early after T. cruzi infection [75]. TS involvement as a neuroprotective factor is also proposed [76]. A strict correlation between the amount of TS shed into the bloodstream and the extent of pathogenesis induced by different T. cruzi strains was observed in experimental infections [77].…”

Section: Trans-sialidase and Mucins: The Yin And Yang Of The Trypomasmentioning

confidence: 99%

The Trypanosoma cruzi Surface, a Nanoscale Patchwork Quilt

Mucci

Lantos

Buscaglia

et al. 2017

Trends in Parasitology

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The Trypanosoma cruzi trypomastigote membrane provides a major protective role against mammalian host-derived defense mechanisms while allowing the parasite to interact with different cell types and trigger pathogenesis. This surface has been historically appreciated as a rather unstructured ‘coat’, mainly consisting of a continuous layer of glycolipids and heavily O-glycosylated mucins, occasionally intercalated with different developmentally-regulated molecules displaying adhesive and/or enzymatic properties. Recent findings, however, indicate that the trypomastigote membrane is made up of multiple, densely packed and discrete 10–150 nm lipid-driven domains bearing different protein composition; hence resembling a highly organized ‘patchwork quilt’ design. Here, we discuss different aspects underlying the biogenesis, assembly and dynamics of this cutting edge fashion outfit, as well as its functional implications.

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“…The importance of the ENS is highlighted by congenital and acquired conditions in which developmental failure (Hirschsprung disease, also referred to as HSCR) or secondary loss (e.g., Chagas disease) of enteric ganglia leads to severe gut dysmotility (6,7). In addition to those conditions in which digestive abnormalities can be clearly ascribed to deficits in enteric ganglia, other often debilitating disorders characterized by disturbed intestinal motor function, such as chronic intestinal pseudo-obstruction or irritable bowel syndrome, present with either inconsistent pathology of the ENS or show no changes in the number or organization of enteric ganglia (8,9).…”

Section: Introductionmentioning

confidence: 99%

Planar cell polarity genes control the connectivity of enteric neurons

Sasselli¹,

Boesmans²,

Berghe³

et al. 2013

J. Clin. Invest.

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A highly complex network of intrinsic enteric neurons is required for the digestive and homeostatic functions of the gut. Nevertheless, the genetic and molecular mechanisms that regulate their assembly into functional neuronal circuits are currently unknown. Here we report that the planar cell polarity (PCP) genes Celsr3 and Fzd3 are required during murine embryogenesis to specifically control the guidance and growth of enteric neuronal projections relative to the longitudinal and radial gut axes. Ablation of these genes disrupts the normal organization of nascent neuronal projections, leading to subtle changes of axonal tract configuration in the mature enteric nervous system (ENS), but profound abnormalities in gastrointestinal motility. Our data argue that PCP-dependent modules of connectivity established at early stages of enteric neurogenesis control gastrointestinal function in adult animals and provide the first evidence that developmental deficits in ENS wiring may contribute to the pathogenesis of idiopathic bowel disorders.

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Neurodegeneration and Neuroregeneration in Chagas Disease

Cited by 30 publications

References 226 publications

Mechanisms of Trypanosoma cruzi persistence in Chagas disease

Mechanisms of Trypanosoma cruzi persistence in Chagas disease

The Trypanosoma cruzi Surface, a Nanoscale Patchwork Quilt

Planar cell polarity genes control the connectivity of enteric neurons

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