Mus musculus
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ABSTRACT:
PROVIDER: PRJNA141541 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression Data from Toxoplasma gondii Infected Murine Bone Marrow-Derived Macrophages
| PRJNA141415 | ENA
Project description:To study the effect of stress on macrophages due to Toxoplasma, we stimulated murine bone marrow-derived macrophages (BMDMs) with IFN-γ (no-stimulate control) and infected them with the apicomplexan parasite Toxoplasma gondii. scRNA-Seq (10X Chromium genomics ) was performed to understand the changes in the immune cells and study the impact of the parasite.
2024-10-09 | E-MTAB-14453 | biostudies-arrayexpress
Project description:Gene expression Data from Toxoplasma gondii-Infected Murine Bone Marrow-Derived STAT6 and STAT3 Deficient Macrophages
| PRJNA193443 | ENA
Project description:Differential macrophage activation mediate genetic differences to a variety of inflammatory pathologies. We wanted to elucidate the transcriptional and regulatory programs regulating differential macrophage activation in genetically diverse mouse strains. Bone marrow-derived macrophages (BMDMs) from AJ and C57BL/6j mice were left unstimulated, stimulated with IFN/TNF, or IL-4, or CpG, or LPS or IFN/TNF and infected with a type II (Pru A7) strain of Toxoplasma gondii, or infected with Pru A7 and gene expression analyzed 18 hrs later.
2013-05-18 | E-GEOD-47046 | biostudies-arrayexpress
Project description:The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (?) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (?/?) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits type I interferon responses when targeted to the host endo-lysosomal system. While live Toxoplasma fails to induce type I interferon, heat-killed parasites do trigger this response, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that some parasite species, like Toxoplasma gondii, have evolved mechanisms to suppress this response. In vitro cultures of bone marrow-derived macrophages from WT or IFNAR2-/- mice were infected with either Toxoplasma gondii (VEG strain) or Neospora caninum (Nc2 strain) for 17 hours. RNA was collected from biological replicates for expression profiling by microarray. Uninfected controls for both WT and IFNAR2-/- were used as a reference.
2013-03-29 | E-GEOD-45632 | biostudies-arrayexpress
Project description:Expression Data from Toxoplasma gondii Infected Murine Macrophages and Dendritic Cells
| PRJNA141419 | ENA
Project description:Intracellular pathogens including the apicomplexan and opportunistic parasite Toxoplasma gondii profoundly modify their host cells in order to establish infection. We have shown previously that intracellular T. gondii inhibit up-regulation of regulatory and effector functions in murine macrophages (MΦ) stimulated with interferon (IFN)-γ, which is the cytokine crucial for controlling the parasites’ replication. Using genome-wide transcriptome analysis we show herein that infection with T. gondii leads to global unresponsiveness of murine macrophages to IFN-γ. More than 61% and 89% of the transcripts, which were induced or repressed by IFN-γ in non-infected MΦ, respectively, were not altered after stimulation of T. gondii-infected cells with IFN-γ. These genes are involved in a variety of biological processes, which are mostly but not exclusively related to immune responses. Analyses of the underlying mechanisms revealed that IFN-γ-triggered nuclear translocation of STAT1 still occurred in Toxoplasma-infected MΦ. However, STAT1 bound aberrantly to oligonucleotides containing the IFN-γ-responsive gamma-activated site (GAS) consensus sequence. Conversely, IFN-γ did not induce formation of active GAS-STAT1 complexes in nuclear extracts from infected MΦ. Mass spectrometry of protein complexes bound to GAS oligonucleotides showed that T. gondii-infected MΦ are unable to recruit non-muscle actin to IFN-γ-responsive DNA sequences, which appeared to be independent of stimulation with IFN-γ and of STAT1 binding. IFN-γ-induced recruitment of BRG-1 and acetylation of core histones at the IFN-γ-regulated CIITA promoter IV, but not β-actin was diminished by >90% in Toxoplasma-infected MΦ as compared to non-infected control cells. Remarkably, treatment with histone deacetylase inhibitors restored the ability of infected macrophages to express the IFN-γ regulated genes H2-A/E and CIITA. Taken together, these results indicate that Toxoplasma-infected MΦ are unable to respond to IFN-γ due to disturbed chromatin remodelling, but can be rescued using histone deacetylase inhibitors. Comparison of 4 different RNA pools with a 2-Color-Loop Design including 10 microarrays: [1] T. gondii infected and IFN-gamma treated, [2] T. gondii infected and untreated, [3] Non-infected and IFN-gamma treated, and [4] Non-infected and untreated.
2012-01-25 | E-GEOD-28499 | biostudies-arrayexpress
Project description:investigate the proximal proteins on the porositophorous vacuole membranes when toxoplasma gondii ME49 infected mouse bone marrow derived dendritic cells were primed under different conditions. The priming condition using IFN gamma will induce the formation of GBP+ puncta on a portion of PVM. The constituents of the GBP+ puncta are also investigated.
2024-02-14 | PXD027716 | Pride
Project description:mRNA-seq of immortailized bone marrow derived macrophages (iBMDM) infected with type II Toxoplasma gondii
| PRJNA528791 | ENA
Project description:Toxoplasma gondii, the causative agent of toxoplasmosis, is an obligate intracellular protozoan parasite that resides inside a parasitophorous vacuole. During infection, Toxoplasma actively remodels the transcriptome of its hosting cells with profound and coupled impact on the host immune response. We report that Toxoplasma secretes GRA24, a novel dense granule protein which traffics from the vacuole to the host cell nucleus. Once released into the host cell, GRA24 has the unique ability to trigger prolonged autophosphorylation and nuclear translocation of the host cell p38M-NM-1 MAP kinase. This noncanonical kinetics of p38M-NM-1 activation correlates with the up-regulation of the transcription factors Egr-1 and c-Fos and the correlated synthesis of key proinflammatory cytokines, including interleukin-12 and the chemokine MCP-1, both known to control early parasite replication in vivo. Remarkably, the GRA24-p38M-NM-1 complex is defined by peculiar structural features and uncovers a new regulatory signaling path distinct from the MAPK signaling cascade and otherwise commonly activated by stress-related stimuli or various intracellular microbes. GRA24 = PSP7 Mouse bone marrow-derived macrophages (BMDM) were infected with the following Toxoplasma gondii strains: - RHku80 WT versus RHku80(deltaPSP7) mutant - Pruku80 WT versus Pruku80(deltaPSP7) mutant
2013-09-01 | E-GEOD-38782 | biostudies-arrayexpress