High Circulating Levels of Fibronectin and Antibodies against Its RGD Adhesion Site during Mouse Trypanosoma cruzi Infection: Relation to Survival

1995 ◽  
Vol 80 (3) ◽  
pp. 499-506 ◽  
Author(s):  
C. Truyens ◽  
M.T. Rivera ◽  
A. Ouaissi ◽  
Y. Carlier
Keyword(s):  
Trypanosoma Cruzi ◽  
Circulating Levels ◽  
Cruzi Infection ◽  
Adhesion Site

scholarly journals Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

2007 ◽  
Vol 204 (4) ◽  
pp. 929-940 ◽  
Author(s):  
Anthony W. Ashton ◽  
Shankar Mukherjee ◽  
FNU Nagajyothi ◽  
Huan Huang ◽  
Vicki L. Braunstein ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Treatment Options ◽  
Thromboxane A2 ◽  
Cardiac Pathology ◽  
Liquid Chromatography Tandem Mass ◽  
Primary Determinant ◽  
Txa2 Receptor ◽  
Circulating Levels ◽  
Cruzi Infection

Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A2 (TXA2). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA2 is the predominant eicosanoid present in all life stages of T. cruzi. Parasite-derived TXA2 accounts for up to 90% of the circulating levels of TXA2 in infected wild-type mice, and perturbs host physiology. Mice in which the gene for the TXA2 receptor (TP) has been deleted, exhibited higher mortality and more severe cardiac pathology and parasitism (fourfold) than WT mice after infection. Conversely, deletion of the TXA2 synthase gene had no effect on survival or disease severity. TP expression on somatic cells, but not cells involved in either acquired or innate immunity, was the primary determinant of disease progression. The higher intracellular parasitism observed in TP-null ECs was ablated upon restoration of TP expression. We conclude that the host response to parasite-derived TXA2 in T. cruzi infection is possibly an important determinant of mortality and parasitism. A deeper understanding of the role of TXA2 may result in novel therapeutic targets for a disease with limited treatment options.

Dynamics of T Cells Repertoire During Trypanosoma cruzi Infection and its Post-Treatment Modulation

2019 ◽  
Vol 26 (36) ◽  
pp. 6519-6543 ◽  
Author(s):  
Adriana Egui ◽  
Paola Lasso ◽  
Elena Pérez-Antón ◽  
M. Carmen Thomas ◽  
Manuel Carlos López
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Cardiac Tissue ◽  
Acute Infection ◽  
Clinical Status ◽  
Chronic Phase ◽  
Parasite Load ◽  
Chronic Patients ◽  
Cruzi Infection

Chagas disease courses with different clinical phases and has a variable clinical presentation and progression. The acute infection phase mostly exhibits a non-specific symptomatology. In the absence of treatment, the acute phase is followed by a chronic phase, which is initially asymptomatic. This chronic asymptomatic phase of the disease is characterized by a fragile balance between the host’s immune response and the parasite replication. The loss of this balance is crucial for the progression of the sickness. The virulence and tropism of the T. cruzi infecting strain together to the inflammation processes in the cardiac tissue are the main factors for the establishment and severity of the cardiomyopathy. The efficacy of treatment in chronic Chagas disease patients is controversial. However, several studies carried out in chronic patients demonstrated that antiparasitic treatment reduces parasite load in the bloodstream and leads to an improvement in the immune response against the Trypanosoma cruzi parasite. The present review is mainly focused on the cellular patterns associated to the clinical status and the evolution of the disease in chronic patients, as well as the effectiveness of the treatment related to T. cruzi infection control. Therefore, an emphasis is placed on the dynamics of specific-antigens T cell subpopulations, their memory and activation phenotypes, their functionality and their contribution to pathogenesis or disease control, as well as their association with risk of congenital transmission of the parasite.

Trypanosoma cruzi Infection Induces Myocardial Nitric Oxide Synthase

1997 ◽  
Vol 6 (3) ◽  
pp. 161-166 ◽  
Author(s):  
Huan Huang, MD ◽  
John Chan, MD ◽  
Murray Wittner, MD, PhD ◽  
Louis M Weiss, MD, MPH ◽  
J Bacchi, PhD ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Trypanosoma Cruzi ◽  
Oxide Synthase ◽  
Cruzi Infection

scholarly journals Real-time PCR strategy for parasite quantification in blood and tissue samples of experimental Trypanosoma cruzi infection

Acta Tropica ◽  
2012 ◽  
Vol 123 (3) ◽  
pp. 170-177 ◽  
Author(s):  
Sérgio Caldas ◽  
Ivo Santana Caldas ◽  
Lívia de Figueiredo Diniz ◽  
Wanderson Geraldo de Lima ◽  
Riva de Paula Oliveira ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Real Time ◽  
Real Time Pcr ◽  
Tissue Samples ◽  
Cruzi Infection

scholarly journals Sialic acid removal by trans-sialidase modulates MMP-2 activity during Trypanosoma cruzi infection

Biochimie ◽  
2021 ◽  
Vol 186 ◽  
pp. 82-93
Author(s):  
Daniel Musikant ◽  
Romina Higa ◽  
Cristina E. Rodríguez ◽  
Martin M. Edreira ◽  
Oscar Campetella ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Trypanosoma Cruzi ◽  
Cruzi Infection
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