scholarly journals Role of Proteomics in the Study of Trypanosoma cruzi Biology

2019 ◽  
Author(s):  
Juan San Francisco ◽  
Bessy Gutiérrez ◽  
Jorge González
Keyword(s):  
Trypanosoma Cruzi

scholarly journals Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Marcela Hernández-Torres ◽  
Rogério Silva do Nascimento ◽  
Monica Cardozo Rebouças ◽  
Alexandra Cassado ◽  
Kely Catarine Matteucci ◽  
...  
Keyword(s):  
T Cells ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Parasite Load ◽  
Peritoneal Macrophages ◽  
T Cell Response ◽  
No Production ◽  
Similar Reduction ◽  
Ifn Γ

AbstractChagas disease is a life-threatening disorder caused by the protozoan parasite Trypanosoma cruzi. Parasite-specific antibodies, CD8+ T cells, as well as IFN-γ and nitric oxide (NO) are key elements of the adaptive and innate immunity against the extracellular and intracellular forms of the parasite. Bim is a potent pro-apoptotic member of the Bcl-2 family implicated in different aspects of the immune regulation, such as negative selection of self-reactive thymocytes and elimination of antigen-specific T cells at the end of an immune response. Interestingly, the role of Bim during infections remains largely unidentified. To explore the role of Bim in Chagas disease, we infected WT, Bim+/−, Bim−/− mice with trypomastigotes forms of the Y strain of T. cruzi. Strikingly, our data revealed that Bim−/− mice exhibit a delay in the development of parasitemia followed by a deficiency in the control of parasite load in the bloodstream and a decreased survival compared to WT and Bim+/− mice. At the peak of parasitemia, peritoneal macrophages of Bim−/− mice exhibit decreased NO production, which correlated with a decrease in the pro-inflammatory Small Peritoneal Macrophage (SPM) subset. A similar reduction in NO secretion, as well as in the pro-inflammatory cytokines IFN-γ and IL-6, was also observed in Bim−/− splenocytes. Moreover, an impaired anti-T. cruzi CD8+ T-cell response was found in Bim−/− mice at this time point. Taken together, our results suggest that these alterations may contribute to the establishment of a delayed yet enlarged parasitic load observed at day 9 after infection of Bim−/− mice and place Bim as an important protein in the control of T. cruzi infections.

scholarly journals The Role of the Trypanosoma cruzi TcNRBD1 Protein in Translation

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0164650 ◽  
Author(s):  
Camila Oliveira ◽  
Paulo Costa Carvalho ◽  
Lysangela Ronalte Alves ◽  
Samuel Goldenberg
Keyword(s):  
Trypanosoma Cruzi

scholarly journals Role of Complement in Immune Lysis of Trypanosoma cruzi

1972 ◽  
Vol 6 (5) ◽  
pp. 860-864 ◽  
Author(s):  
Dante F. Anziano ◽  
Agustin P. Dalmasso ◽  
Rosalia Lelchuk ◽  
César Vásquez
Keyword(s):  
Trypanosoma Cruzi

scholarly journals Role of endothelin receptors in the control of central nervous system parasitism in Trypanosoma cruzi infection in rats

2010 ◽  
Vol 220 (1-2) ◽  
pp. 64-68 ◽  
Author(s):  
Milene A. Rachid ◽  
Antônio L. Teixeira ◽  
Lucíola S. Barcelos ◽  
Conceição R.S. Machado ◽  
Egler Chiari ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Trypanosoma Cruzi ◽  
Endothelin Receptors ◽  
Cruzi Infection

scholarly journals The Role of Acidocalcisomes in the Stress Response of Trypanosoma cruzi

2011 ◽  
pp. 307-324 ◽  
Author(s):  
Roberto Docampo ◽  
Veronica Jimenez ◽  
Sharon King-Keller ◽  
Zhu-hong Li ◽  
Silvia N.J. Moreno
Keyword(s):  
Stress Response ◽  
Trypanosoma Cruzi

scholarly journals Correction to: The role of fat on cardiomyopathy outcome in mouse models of chronic Trypanosoma cruzi infection

2020 ◽  
Vol 119 (6) ◽  
pp. 1845-1845
Author(s):  
Paul Zaki ◽  
Elisa L. B. C. Domingues ◽  
Farhad M. Amjad ◽  
Maiara B. Narde ◽  
Karolina R. Gonçalves ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Mouse Models ◽  
Cruzi Infection

scholarly journals Characterization of Trypanosoma cruzi Sirtuins as Possible Drug Targets for Chagas Disease

2015 ◽  
Vol 59 (8) ◽  
pp. 4669-4679 ◽  
Author(s):  
Nilmar Silvio Moretti ◽  
Leonardo da Silva Augusto ◽  
Tatiana Mordente Clemente ◽  
Raysa Paes Pinto Antunes ◽  
Nobuko Yoshida ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Drug Targets ◽  
Wild Type ◽  
Content Type ◽  
Damage Repair ◽  
Lysine Deacetylases

ABSTRACTAcetylation of lysine is a major posttranslational modification of proteins and is catalyzed by lysine acetyltransferases, while lysine deacetylases remove acetyl groups. Among the deacetylases, the sirtuins are NAD+-dependent enzymes, which modulate gene silencing, DNA damage repair, and several metabolic processes. As sirtuin-specific inhibitors have been proposed as drugs for inhibiting the proliferation of tumor cells, in this study, we investigated the role of these inhibitors in the growth and differentiation ofTrypanosoma cruzi, the agent of Chagas disease. We found that the use of salermide during parasite infection prevented growth and initial multiplication after mammalian cell invasion byT. cruziat concentrations that did not affect host cell viability. In addition,in vivoinfection was partially controlled upon administration of salermide. There are two sirtuins inT. cruzi, TcSir2rp1 and TcSir2rp3. By using specific antibodies and cell lines overexpressing the tagged versions of these enzymes, we found that TcSir2rp1 is localized in the cytosol and TcSir2rp3 in the mitochondrion. TcSir2rp1 overexpression acts to impair parasite growth and differentiation, whereas the wild-type version of TcSir2rp3 and not an enzyme mutated in the active site improves both. The effects observed with TcSir2rp3 were fully reverted by adding salermide, which inhibited TcSir2rp3 expressed inEscherichia coliwith a 50% inhibitory concentration (IC50) ± standard error of 1 ± 0.5 μM. We concluded that sirtuin inhibitors targeting TcSir2rp3 could be used in Chagas disease chemotherapy.

scholarly journals Lysosomal Fusion Is Essential for the Retention of Trypanosoma cruzi Inside Host Cells

2004 ◽  
Vol 200 (9) ◽  
pp. 1135-1143 ◽  
Author(s):  
Luciana O. Andrade ◽  
Norma W. Andrews
Keyword(s):  
Plasma Membrane ◽  
Life Cycle ◽  
Trypanosoma Cruzi ◽  
Parasitophorous Vacuole ◽  
Cell Types ◽  
Significant Fraction ◽  
Host Cells ◽  
Productive Infection ◽  
Kinase Inhibition

Trypomastigotes, the highly motile infective forms of Trypanosoma cruzi, are capable of infecting several cell types. Invasion occurs either by direct recruitment and fusion of lysosomes at the plasma membrane, or through invagination of the plasma membrane followed by intracellular fusion with lysosomes. The lysosome-like parasitophorous vacuole is subsequently disrupted, releasing the parasites for replication in the cytosol. The role of this early residence within lysosomes in the intracellular cycle of T. cruzi has remained unclear. For several other cytosolic pathogens, survival inside host cells depends on an early escape from phagosomes before lysosomal fusion. Here, we show that when lysosome-mediated T. cruzi invasion is blocked through phosophoinositide 3-kinase inhibition, a significant fraction of the internalized parasites are not subsequently retained inside host cells for a productive infection. A direct correlation was observed between the lysosomal fusion rates after invasion and the intracellular retention of trypomastigotes. Thus, formation of a parasitophorous vacuole with lysosomal properties is essential for preventing these highly motile parasites from exiting host cells and for allowing completion of the intracellular life cycle.

Trypanosoma cruzi: death phenotypes induced by ortho-naphthoquinone substrates of the aldo-keto reductase (TcAKR). Role of this enzyme in the mechanism of action of β-lapachone

Parasitology ◽  
2018 ◽  
Vol 145 (9) ◽  
pp. 1251-1259 ◽  
Author(s):  
Patricia Andrea Garavaglia ◽  
María Fernanda Rubio ◽  
Marc Laverrière ◽  
Laura Mónica Tasso ◽  
Laura Edith Fichera ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Mitochondrial Membrane ◽  
Major Influence ◽  
Ros Production ◽  
Oxygen Species ◽  
Aetiological Agent ◽  
Toxicity Evaluation

AbstractSeveral ortho-naphthoquinones (o-NQs) have trypanocidal activity against Trypanosoma cruzi, the aetiological agent of Chagas disease. Previously, we demonstrated that the aldo-keto reductase from this parasite (TcAKR) reduces o-NQs, such as β-lapachone (β-Lap) and 9,10-phenanthrenequinone (9,10-PQ), with concomitant reactive oxygen species (ROS) production. Recent characterization of TcAKR activity and expression in two T. cruzi strains, CL Brener and Nicaragua, showed that TcAKR expression is 2.2-fold higher in CL Brener than in Nicaragua. Here, we studied the trypanocidal effect and induction of several death phenotypes by β-Lap and 9,10-PQ in epimastigotes of these two strains. The CL Brener strain was more resistant to both o-NQs than Nicaragua, indicating that greater TcAKR activity is unlikely to be a major influence on o-NQ toxicity. Evaluation of changes in ROS production, mitochondrial membrane potential, phosphatidylserine exposure and monodansylcadaverine labelling evidenced that β-Lap and 9,10-PQ induce different death phenotypes depending on the combination of drug and T. cruzi strain analysed. To study whether TcAKR participates in o-NQ activation in intact parasites, β-Lap and 9,10-PQ trypanocidal effect was next evaluated in TcAKR-overexpressing parasites. Only β-Lap was more effective and induced greater ROS production in TcAKR-overexpressing epimastigotes than in controls, suggesting that TcAKR may participate in β-Lap activation.

Cytokine modulation, oxidative stress and thymic dysfunctions: Role of age-related changes in the experimental Trypanosoma cruzi infection

Cytokine ◽  
2018 ◽  
Vol 111 ◽  
pp. 88-96 ◽  
Author(s):  
Rafaela Pravato Colato ◽  
Vânia Brazão ◽  
Gabriel Tavares do Vale ◽  
Fabricia Helena Santello ◽  
Pedro Alexandre Sampaio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Trypanosoma Cruzi ◽  
Cytokine Modulation ◽  
Age Related ◽  
Cruzi Infection ◽  
Age Related Changes
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