Ontology highlight
ABSTRACT:
PROVIDER: PRJNA552423 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE25468: Expression data from Human foreskin fibroblasts (HFFs) infected with Toxoplasma gondii. GSE25469: Expression data from WT or p65-/- mouse embryonic fibroblasts (MEFs) infected with Toxoplasma gondii. Refer to individual Series
2011-01-10 | E-GEOD-25476 | biostudies-arrayexpress
Project description:To identify accessible chromatin regions in the human host cells during Toxoplasma parasite infection (uninfected, RH-infected and Pru-infected human foreskin fibroblasts) and in the obligate intracellular parasite Toxoplasma gondii (Type 1 RH strain and Type 2 Pru strain), ATAC-seq was performed.
2022-09-30 | GSE209866 | GEO
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:Analysis of Ly6Chi monocytes from small intestine lamina propria (SILP) and blood of day 8 Toxoplasma gondii infected mice at gene expression level. The hypothesis tested in the present study was that Ly6Chi monocytes from SILP have altered expression of regulatory factors to blood monocytes. Results provide important information on the regulatory to effector balance of genes expressed by Ly6Chi monocytes during an acute inflammatory response. Ly6Chi inflammatory monocytes were sorted by FACS from the blood or small intestine lamina propria (SILP) of Toxoplasma gondii infected C57BL/6 mice. Cells were isolated at day 8 after infection and total RNA obtained from sorted populations. Three biological replicates were acquired for both blood and SILP from pooled animals.
2013-05-25 | E-GEOD-46685 | biostudies-arrayexpress
Project description:The in vitro effect of infection with different strains of Toxoplasma gondii was tested 24 hours after infection of Human Foreskin Fibroblasts (HFF) The strains tested include RH, VEG, and transgenic strains of RH overexpressing ROP38 or ROP21 Total RNA of Toxoplasma gondii infected HFF cell was compared to uninfected cells
2010-07-31 | E-GEOD-22402 | biostudies-arrayexpress
Project description:Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that can infect almost all warm-blooded animals, causing serious public health problems. Lysine crotonylation (Kcr) is a newly discovered posttranslational modification (PTM), which has been proved that is relevant to procreation regulation, active transcription and cell signaling pathway. However, the biological functions of crotonylation have not yet been reported in macrophages infected with T. gondii. In our study, we performed a ChIP-seq analysis of porcine alveolar macrophages infected with T. gondii RH to explore the relationship of histone Kcr with T. gondii infection.
2021-12-31 | GSE167340 | GEO
Project description:Expression profile microarray of human foreskin fibroblast cell comparing control untreated HFF cell with HFF cell infected with ME49 strain.Study on Toxoplasma gondii infection of HFF cell LncRNAs expression, for further studies on the differential exprssion of LncRNAs in HFF cell against the infection of Toxoplasma gondii research provide the basic function.
2017-01-01 | GSE92603 | GEO
Project description:Toxoplasma gondii is an apicomplexan parasite infecting human and animals, causing huge health concerns and economic losses. However, it is unclear about the exact mechanism of T.gondii tachyzoite infected macrophage and macrophage resisted T.gondii, especially for local isolates such as TgHB1 isolated in China. Our study focused on the transcriptional difference of pig alveolar macrophages (3D4/21) infected with china isolated TgHB1 compared to TgRH and TgME49 toxoplasma gondii standard strains.
2020-09-12 | GSE153330 | GEO
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 (γ) 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 (α/β) 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. Human foreskin fibroblasts (HFF; line BJ-5ta) were cultured to confluency in T25 flasks, infected with one representative of each of the three architypial strains of Toxoplasma gondii: GT1 (type I), Prugniaud (type II) and VEG (type III), or the closely related parasite species, Neospora caninum (strain Nc-Liv). RNA was collected from biological replicates for expression profiling by microarray. Uninfected HFF cells were used as a reference.
2013-03-29 | E-GEOD-45633 | biostudies-arrayexpress
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