Project description:This project aims to investigate the immuno-physiology of the Chagas disease vector Rhodnius prolixus, by analysing the effect of blood ingestion and Trypanosoma cruzi colonisation of its digestive tract on the modulation of protein expression in the hemolymph.
Project description:Rhodnius prolixus are insect triatomines and vectors of the protozoan Trypanosoma cruzi responsible for human Chagas' disease. Considering that T. cruzi multiplies inside the triatomine digestive tract (TDT), the analysis of the TDT protein profile is an essential step to understand TDT physiology during T. cruzi infection. To characterize the protein profile of TDT of R. prolixus, a shotgun liquid chromatography-tandem mass spectrometry (LC-MS/MS) approach was applied in this report.
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
Project description:Analysis of the effect of Trypanosoma cruzi establishment in the anterior midgut of its vector, Rhodnius prolixus, on the variation of its protein expression after 6 and 24 hours post-infection
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis). We are working with an enzyme able to directly transfer sialyl residues among macromolecules known as the trans-sialidase. It constitutes a virulence factor from Trypanosoma cruzi, the agent of the Chagas' Disease the American trypanosomiasis. We described the ability of this virulence factor to induce thymocyte apoptosis in vivo that happens after silayl residue mobilization. The apoptosis is mediated by the thymic epithelial cells in the nurse cell complex. By employing the microarray approach we wish to analyze the gene expression induced in the thymus after TS treatment. Examination of differential expression in thymocytes between male and female mice of genes related to glycosylation. RNA samples (in triplicate) purified from thymocytes were analyzed by Glyco-gene Chip analysis.
Project description:An efficient innate immune recognition of the intracellular parasite T. cruzi is crucial for host protection against development of Chagas disease, which often leads to multiple organ damage, particularly the heart leading to cardiomyopathy. Mechanisms modulated by MyD88 have been shown to be necessary for resistance against T, cruzi infection. Recently, Nod-like receptors have been shown to play an important role as innate immune sensors, particularly as they relate to inflammasome function, caspase activation, and inflammatory cytokine production. In this study, we aimed to investigate the participation of innate immune responses in general, and inflammasomes in particular, in heart inflammation and cardiac damage upon infection with the T. cruzi parasite. We used microarrays to gain insight into gene expression in the cardiac tissue of mice infected with the causative agent of Trypanosoma cruzi, and identified distinct classes of up-regulated genes during this process, including important genes involved in inflammasome activation and innate immune responses in general.
Project description:Chagas disease is a parasitic infection originally endemic to latinamerican countries but now spreaded worldwide that can be transmitted congenitally. Current specific therapy involves benznidazole, however, other therapies may modify gene expression that can change genetic expression profile, allowing cell programming to provide a more unfavorable environment for intracellular parasite development. Herein, microarray analysis was performed to Human Umbilical Vein Endothelial Cells (HUVEC), treated with benznidazole and the anti-inflammatory drugs aspirin or simvastatin, and infected with T. cruzi, the causative agent of Chagas disease.
Project description:We studied the impact of the gene knockout of the TcK2 protein kinase of Trypanosoma cruzi, the causative agent of Chagas disease. TcK2 is structurally similar to the human kinase PERK, which phosphorylates the initiation factor eIF2alpha, and in turn, inhibits translation initiation. As TcK2 kinase promotes parasite proliferation within mammalian cell, it is a potential target for treatment of Chagas disease. Proteomics indicates that proliferative forms express genes including trans-sialidases, normally restricted to infective and non-proliferative trypomastigotes. In addition, TcK2 knockout cells lose phosphorylation of eukaryotic initiation factor 3 and cyclic AMP responsive-like element, recognized to promote growth, likely explaining both decreased proliferation and augmented differentiation.
Project description:An efficient innate immune recognition of the intracellular parasite T. cruzi is crucial for host protection against development of Chagas disease, which often leads to multiple organ damage, particularly the heart leading to cardiomyopathy. Mechanisms modulated by MyD88 have been shown to be necessary for resistance against T, cruzi infection. Recently, Nod-like receptors have been shown to play an important role as innate immune sensors, particularly as they relate to inflammasome function, caspase activation, and inflammatory cytokine production. In this study, we aimed to investigate the participation of innate immune responses in general, and inflammasomes in particular, in heart inflammation and cardiac damage upon infection with the T. cruzi parasite. We used microarrays to gain insight into gene expression in the cardiac tissue of mice infected with the causative agent of Trypanosoma cruzi, and identified distinct classes of up-regulated genes during this process, including important genes involved in inflammasome activation and innate immune responses in general. The hearts of C57BL/6 mice day 18 post-infection with a Y strain of the parasite T. cruzi, and uninfected controls were extraced for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare gene expression among two groups of mice, and so extracted the hearts of 3 control uninfected mice, and of 3 infected mice 18 days post-infection.