GNPS_Determinants of Chagas disease progression
Ontology highlight
ABSTRACT:
INSTRUMENT(S): micrOTOF-Q II
ORGANISM(S): Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
Laura-Isobel McCall James McKerrow
PROVIDER: MSV000079615 | GNPS | Tue Mar 29 12:44:00 BST 2016
REPOSITORIES: GNPS
Similar Datasets
Project description:Multiplexed, quantitative proteomics and phosphoproteomics of mouse hearts infected with Trypanosoma cruzi - Chagas Disease cardiomyopathy
2019-08-09 | MSV000084188 | MassIVE
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.
2012-11-20 | E-GEOD-41089 | biostudies-arrayexpress
Project description:Investigate transcriptional responses of T. cruzi infected hiPSC-derived cardiomyocytes from chagasic patients with and without cardiomyopathy.
2022-06-20 | GSE203525 | GEO
Project description:Mice were infected with Trypanosoma cruzi strains CL, X10/4 or X10/7. Hearts were collected 12 days, 3 months and 5 months post-infection from infected mice and uninfected age-matched controlled. Hearts were divided into four sections from the base of the heart to the apex. Metabolites were extracted by a two-step protocol, first with 50% methanol (aqueous extract) then with 3:1 dichloromethane:methanol (organic extract). Liquid chromatography separation was performed on a Kinetex C8 LC Column 50 x 2.1 mm, with water+0.1% formic acid and acetonitrile+0.1% formic acid as mobile phases.
2017-01-05 | MSV000080450 | GNPS
Project description:Mice were infected with Trypanosoma cruzi parasites, followed by treatment with benznidazole. Controls include uninfected mice and mice treated with isoproterenol to induce cardiac failure through chemical mechanisms. Urine was collected pre- and post-treatment and extracted using methanol, followed by LC separation using polar C18 LC and positive mode MS/MS data acquisition.
2021-11-23 | MSV000088436 | GNPS
Project description:Comparative genomic analysis of Trypanosoma cruzi G with Trypanosoma cruzi D11.
2022-03-06 | GSE197870 | GEO
Project description:Fecal samples were collected from Trypanosoma cruzi-infected (strain CL+Luc) and uninfected mice for up to 3 months post-infection. Samples were extracted with 50% methanol.
2017-04-21 | MSV000080976 | GNPS
Project description:These assays represent an antigen discovery screening, and epitope mapping characterization. In this screening two complete proteomes from Trypanosoma cruzi, from two different strains (CL-Brener, Sylvio X10), were displayed in the form of short peptides (tiling array, overlapped) and assayed with pooled serum samples (antibodies) from Chagas Disease patients and matched negative (healthy) subjects selected from 6 geographic regions across the Americas. Peptide arrays (slides) were incubated with pooled serum samples (primary antibodies), washed, and then incubated with a fluorescently-labeled anti-human IgG commercial antibody (secondary antibodies). Raw readouts of fluoresence (signal), as well as normalized signal values are provided in this submission for all samples analyzed. All samples were analyzed in duplicate.
2022-08-20 | E-MTAB-11651 | biostudies-arrayexpress
Project description:To investigate the early host response triggered by three different strains of Trypanosoma cruzi at a local infection site, changes in host gene expression were monitored in a murine intradermal infection model using Affymetrix oligonucleotide arrays. Robust induction of IFN-stimulated genes (ISGs) was observed in excised skin 24 hours post-infection where the level of ISG induction was parasite strain-dependent with the least virulent strain triggering a muted IFN response. Infection of mice immunodepleted of IFNγ-producing cells or infection of IFNγ-deficient mice had minimal impact on the IFN response generated in T. cruzi infected mice. In contrast, infection of mice lacking the type I IFN receptor demonstrated that type I IFNs are largely responsible for the IFN response generated at the site of infection. These data highlight type I IFNs as important components of the innate immune response to T. cruzi the site of inoculation and their role in shaping the early transcriptional response to this pathogen. We used microarrays to detail the local host transcriptional response to intradermal T. cruzi infection in WT mice and mice depleted of NK cells, or deficient in IFN-gamma or type I IFN responses. Additionally we compared the local host-transcriptional response generated to infection with 3 different strains of Trypanosoma cruzi (Y, Brazil, and G). Experiment Overall Design: Mice were infected by intradermal injection of 10^6 T. cruzi trypomastigotes in 100uL of saline split between 2 adjacent sites on the shaved side flank. Control mice were injected with an equal volume of saline. 24 hours post-injection approximately 75mm^2 of skin immediately surrounding the injection site was excised and RNA was isolated from the tissue. Balb/c mice were used for most experiments and IFN-gamma KO mice were on the Balb/c background. WT 129 mice were also used as IFNAR-/- mice were on the 129 background. In total 33 arrays were performed. 7 WT (Balb/c) control, 3 Y strain infected, 3 Brazil strain infected, 3 G strain infected, 2 IFN-gamma KO control, 2 IFN-gamma KO infected, 1 NK cell depleted control, 1 NK cell depleted infected, 3 WT (129) control, 3 WT (129) infected, 3 IFNAR KO control, 3 IFNAR KO infected
2009-01-14 | E-GEOD-13522 | biostudies-arrayexpress
Project description:Chagas disease causes a cardiac illness characterized by immunoinflammatory reactions leading to myocardial fibrosis and remodeling. The development of Chronic Chagas Cardiomyopathy (CCC) in some patients while others remain asymptomatic is not fully understood, but dysregulated inflammatory responses are implicated. The Aryl hydrocarbon receptor (AhR) plays a crucial role in regulating inflammation. Certain tryptophan (Trp) metabolites have been identified as AhR ligands with regulatory functions. We investigated AhR expression, agonist response, ligand production, and AhR-dependent responses, such as IDO activation and regulatory T (Treg) cells induction, in two T.cruzi-infected mouse strains (B6 and Balb/c) showing different polymorphisms in AhR. Furthermore, we assessed the metabolic profile of Trp catabolites and AhR agonistic activity levels in plasma samples from patients with chronic Chagas disease (CCD) and healthy donors (HD) using a luciferase reporter assay and liquid chromatography-mass spectrophotometry (LC-MS) analysis. T. cruzi-infected B6 mice showed impaired AhR-dependent responses compared to Balb/c mice, including reduced IDO activity, kynurenine levels, Treg cell induction, CYP1A1 up-regulation, and AhR expression following agonist activation. Additionally, B6 mice exhibited no detectable 34 AhR agonist activity in plasma and displayed lower CYP1A1 up-regulation and AhR expression upon agonist activation. Similarly, CCC patients had decreased AhR agonistic activity in plasma compared to HD patients and exhibited dysregulation in Trp metabolic pathways, resulting in altered plasma metabolite profiles. Notably, patients with severe CCC specifically showed increased N-acetylserotonin levels in their plasma. The methods and findings presented here contribute to a better understanding of CCC development mechanisms and may identify potential specific biomarkers for T. cruzi infection and the severity of associated heart disease. These insights could be valuable in designing new therapeutic strategies. Ultimately, this research aims to establish the AhR agonistic activity and Trp metabolic profile in plasma as an innovative, non-invasive predictor of prognosis for chronic Chagas disease.
2023-10-09 | GSE244478 | GEO