Similar Datasets
Project description:To generate a high quality, annotated gene expression database of T. cruzi trypomastigotes(TRP), amastigotes (AMA), epimastigotes (EPI), and metacyclic trypomastigotes (MET). The global assessment of transcript abundances in each life-cycle stage of T. cruzi will identify stage-regulated genes and provide an essential element of an integrated database of T. cruzi genomic, proteomic, and transcriptomic data. RNAs from 3 biological replicates from a single time point in each stage will be subjected to DNA microarrays containing probes for the complete, annotated T. cruzi genome, as it is currently known. The arrays for this project will be provided by the Pathogen Functional Genomics Resource Center (PFGRC) at The Institute for Genomic Research (TIGR) sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), and will contain long oligonucleotides complementary to every annotated gene in the newly sequenced T. cruzi genome. The resulting data and analysis results will be deposited in TcruziDB (http://TcruziDB.org). Keywords: Gene expression comparisons between the four life-cycle stages of T. cruzi
2009-08-01 | GSE14641 | GEO
Project description:To generate a high quality, annotated gene expression database of T. cruzi trypomastigotes(TRP), amastigotes (AMA), epimastigotes (EPI), and metacyclic trypomastigotes (MET). The global assessment of transcript abundances in each life-cycle stage of T. cruzi will identify stage-regulated genes and provide an essential element of an integrated database of T. cruzi genomic, proteomic, and transcriptomic data. RNAs from 3 biological replicates from a single time point in each stage will be subjected to DNA microarrays containing probes for the complete, annotated T. cruzi genome, as it is currently known. The arrays for this project will be provided by the Pathogen Functional Genomics Resource Center (PFGRC) at The Institute for Genomic Research (TIGR) sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), and will contain long oligonucleotides complementary to every annotated gene in the newly sequenced T. cruzi genome. The resulting data and analysis results will be deposited in TcruziDB (http://TcruziDB.org). Keywords: Gene expression comparisons between the four life-cycle stages of T. cruzi Six hybridizations were performed for each life-cycle stage. The hybridizations consisted of three dye-swap experiments from three independent samples (biological replicates). In each case, the experimental sample was from a single life-cycle stage and the control sample was an equal mixture of all four life-cycle stages. A total of 24 hybridizations were preformed.
2010-05-15 | E-GEOD-14641 | biostudies-arrayexpress
Project description:Comparative transcriptome profiling of virulent and non-virulent Trypanosoma cruzi (trypomastigotes)
| PRJNA389925 | ENA
Project description:Using Endothelial Cells as a Model to Study Trypanosoma cruzi Infection
| PRJNA737289 | ENA
Project description:Oral transmission of T. cruzi is probably the most frequent mechanism among animals in the wild. In this context, there is a high prevalence of human infections in regions where triatomine infection with T. cruzi is low. This led to the hypothesis that the consumption of raw or undercooked meat from animals infected with T. cruzi could be responsible for the transmission of the infection. Therefore, the general objective of this study was to demonstrate the role of meat consumption from infected animals in the oral transmission of T. cruzi infection. Groups of five female mice Balb/c were fed with muscles obtained from mice in the acute phase of infection by the clone H510 C8C3hvir of T. cruzi, and the infection of the fed mice was monitored by a parasitemia curve. Similarly, we assessed the infective capacity of T. cruzi trypomastigotes and amastigotes by infecting groups of five mice Balb/c females, which were infected orally using a nasogastric probe, and the infection was monitored by parasitemia curve. Finally, different trypomastigote and amastigote inoculums were used to determine their infective capacity. Adhesion assays of T. cruzi proteins to AGS stomach cells were performed and the adhered proteins were detected by western blotting using monoclonal or polyclonal antibodies. In all cases, 60–100% of animals were fed meat from mice infected in the acute phase or infected by means of a nasogastric probe with trypomastigotes or amastigotes. These animals developed high parasitemia, and 80% died around day 40 post-infection. The adhesion tests showed that cruzipain is a molecule of trypomastigotes and amastigotes that binds to AGS cells. LC-MS/MS also confirmed that transialidase may be involved in TCT attachment of TCT or invasion of stomach cells. It was concluded that the consumption of meat from infected animals in the acute phase of T. cruzi infection allows transmission of the infection. Similarly, trypomastigotes and amastigotes were able to infect mice when administered orally, while cruzipain was a relevant molecule in this infective process.
2024-05-21 | PXD044267 | Pride
Project description:Trypanosoma cruzi dysregulates the gene expression profile of primary human cardiomyocytes (PHCM) during the early phase of infection through a mechanism which remains to be elucidated. The role that small non-coding RNAs (sncRNA) including PIWI-interacting RNA (piRNA) play in regulating gene expression during the early phase of infection is unknown. To understand how T. cruzi dysregulate gene expression in the heart, we challenged PHCM with T. cruzi trypomastigotes and analyzed sncRNA, especially piRNA, by RNA-sequencing. The parasite induced significant differential expression of host piRNAs. An average of 21,595,866 (88.40%) of clean reads mapped to the human reference genome. The parasite induced 217 unique piRNAs that were significantly differentially expressed (q ≥ 0.8). Of these differentially expressed piRNAs, 6 were known and 211 were novel piRNAs. In silico analysis showed that some of the dysregulated known and novel piRNAs could target and potentially regulate the expression of genes reported to play important roles during T. cruzi infection. This is the first report showing that T. cruzi can induce differential expression of piRNAs in PHCM, advancing our knowledge about the involvement of piRNAs in an infectious disease model.
2021-12-28 | GSE192658 | GEO
Project description:Chagas’ disease, one of the major public health concerns in Latin America, is caused by the haemophlagelated protozoan Trypanosoma cruzi (T. cruzi). In the past few years congenital transmission of T. cruzi has become more important, and partly responsible for the “globalization of Chagas’ disease”. The congenital transmission, although with low rates, represents the main route of transmission in non-endemic countries and endemic countries without vectorial transmission, and represents one third of the new cases each year. Diverse pathogens, including T. cruzi, are able to cross the placental barrier and infect both the placenta and fetus. However, the exact cellular and molecular mechanisms of host-pathogen interaction between T. cruzi and the placenta has been scarcely studied. The use of microarray analysis to determine expression profiles constitutes a powerful tool in order to identify genes and pathways related to the host response to infections. Here, we analyzed the transcriptomic response of human placental chorionic villi explants (HPCVE) challenged with T. cruzi trypomastigotes at low (105) and high (106) concentrations for 2 and 24 hours
2018-04-17 | GSE113155 | GEO
Project description:Trypanosoma cruzi is an obligate intracellular protozoan parasite that causes human Chagas’ disease, a leading cause of heart failure in Latin America. Using Affymetrix oligonucleotide arrays we screened phenotypically diverse human cells (foreskin fibroblasts, microvascular endothelial cells and vascular smooth muscle cells) for a common transcriptional response signature to T. cruzi. A common feature was a prominent type I interferon response, indicative of a secondary response to secreted cytokines. Using transwell plates to distinguish cytokine-dependent and -independent gene expression profiles in T. cruzi-infected cells, a core cytokine-independent response was identified in fibroblasts and endothelial cells that featured metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding. Significant downregulation of genes involved in mitotic cell cycle and cell division predicted that T. cruzi infection impedes cell cycle progression in the host cell.
2009-06-04 | GSE13791 | GEO
Project description:Analysis of interactors of H2B.V and H2B of T. cruzi using samples from epimastigotes and cellular trypomastigotes.
2022-02-07 | PXD026339 | Pride
Project description:Trypanosoma cruzi, a flagellated protozoan, is the causative agent of Chagas’ disease, a chronic and potentially fatal disease that causes irreversible damage to heart and digestive tract in humans. Like all trypanosomes, the protein coding genes of T. cruzi are arranged into large polycistronic gene clusters transcribed by polymerase II (Pol II). Therefore, trypanosomes presumably rely on post-transcriptional process to regulate gene expression. Pol II promoters have not been identified and there is no evidence for regulated gene expression at the transcriptional level. However, the presence of the hyper-modified DNA base J, Beta-D-glucosyl hydroxymethyluracil, at regions flanking the polycistronic units (PTU) in T. brucei suggested its involvement in regulating Pol II transcription. We now demonstrate that base J is localized at PTU flanking regions in T. cruzi and levels are differentially regulated by the thymidine hydroxylases, JBP1 and JBP2, involved in J biosynthesis. Microarray analysis of the JBP1dKO and JBP2dKO indicate the up and down regulation of several hundred genes distributed throughout the genome. We show a large increase in Pol II transcription rate following the decrease in base J at the PTU flanks. Changes in gene expression include virulence genes and parasites are defective in host cell invasion and egress. There is a direct correlation between the reduction in base J levels, number of genes affected and strength of the virulence phenotype. These studies indicate that base J represents an epigenetic factor regulating Pol II transcription initiation in kinetoplastids and provides a biological role of the only hyper-modified DNA base in eukaryotes. J1 and J2 null mutant trypomastigotes were each compared to wild type trypomastigotes. There were 3 biological replicates for each comparison.
2011-01-01 | E-GEOD-23855 | biostudies-arrayexpress