GNPS_Chagas_Disease_Biomarker_Study_positive
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive
ORGANISM(S): Mice
SUBMITTER: 
Laura-Isobel McCall
PROVIDER: MSV000085900 | GNPS | Mon Aug 03 15:18:00 BST 2020
REPOSITORIES: GNPS
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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.
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Project description:Comparative genomic analysis of Trypanosoma cruzi G with Trypanosoma cruzi D11.
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Project description:To provide a global perspective on the relationships between macrophage activation programs and to understand how certain pathogens circumvent them, we used transcriptional profiling by genome wide microarray analysis to compare the responses of mouse macrophages following exposure to the intracellular parasites Trypanosoma cruzi and Leishmania mexicana, the bacterial product lipopolysaccharide (LPS), and the cytokines IFNG, TNF, IFNB, IL-4, IL-10, and IL-17. We found that LPS induced a classical activation state that resembled macrophage stimulation by the Th1 cytokines IFNG and TNF. However, infection by the protozoan pathogen Leishmania mexicana produced so few transcriptional changes that the infected macrophages were almost indistinguishable from uninfected cells. Trypanosoma cruzi activated macrophages produced a transcriptional signature characterized by the induction of interferon-stimulated genes by 24 h post-infection. Despite this delayed IFN response by T. cruzi, the transcriptional response of macrophages infected by the kinetoplastid pathogens more closely resembled the transcriptional response of macrophages stimulated by the cytokines IL-4, IL-10, and IL-17 than macrophages stimulated by Th1 cytokines. Keywords: Bone marrow macrophage response to intracellular parasites and cytokines We analyzed a series MEEBO arrays on which were hybed RNA amplified from bone marrow-derived macrophages from C57BL/6 mice. Macrophages infected with L. mexicana or T. cruzi or stimulated by LPS, IFNG, IL-4, IL-10, TNF, IFNB, or IL-17 were compared to one another as well as to uninfected, unstimulated control macrophages. All experiments were performed over a 24 h timecourse with timepoints taken at 2 h, 6 h, 12 h, and 24 h.
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Project description:Female mice aged 6-7 weeks old were infected with the T. cruzi H1 strain. Mice were randomly divided into groups with 15 animals in each, with age matched naïve mice included as controls. Approximately 75 days post infection, mice were randomly divided into groups and treated with different treatment combinations: BNZ + Tc24 therapeutic vaccine + the STAT-3 inhibitor TTI-101, BNZ + Tc24 vaccine, and BNZ or TTI alone. Mice were humanely euthanized at 50, 75, 120 or 142 days post infection (DPI), and hearts samples were collected, divided into left atrium (LA), right atrium (RA), left ventricle top (LVT), left ventricle bottom (LVB), right ventricle top (RVT), right ventricle bottom (RVB). Heart tissue samples were extracted by 1:1 (v/v) methanol to water for aqueous phase and 3:1 (v/v) dichloromethane to methanol for organic phase. LC-MS/MS data acquisition was performed on a Q Exactive Plus Hybrid Quadrupole-Orbitrap Mass Spectrometer coupled to a Thermo Scientific Vanquish UHPLC with 1.7 um 100 Å Kinetex C8 column at 40°C. Mobile phase A was water with 0.1% (v/v) formic acid and mobile phase B was acetonitrile with 0.1% (v/v) formic acid.
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Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Experiment Overall Design: Three replicates of infected and uninfected HeLa cell were analyzed. To examine the extent of cross hybridization between T. cruzi cRNA and Human chip, trypomastigote cRNA was hybridized with the same chip.
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Project description:Male CD-1 mice (N=8) were intraperitoneally infected by culture-derived Trypanosoma cruzi trypomastigotes of the Brazil strain. One group (N=4) was treated with an antitrypanosomal drug (nifurtimox) on day 74 post-infection (chronic phase) for 20 days. A group of uninfected mice (N=3) was also included as control. All groups (N=11) were enthanized on day 110 post-infection, testes were collected and subjected to 2D-LC-MS/MS analysis. Label-free quantitation revealed that the testes of T. cruzi-infected mice had an altered proteome pattern relative to treated mice and uninfected controls. The analysis also demonstrated that the left and right testes had different proteomic profiles in infected animals.
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