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Expression data from cyclohexamide treated Human Foreskin Fibroblasts (HFFs) infected with type I Toxoplasma gondii and stimulated with interferon gamma.

ABSTRACT: Pre-infection with Toxoplasma parasites inhibits induction of an interferon gamma responsive gene expression program. In this study we aimed to determine what role host negative regulatory proteins that are induced by Toxoplasma infection, such as SOCS-1, have in this inhibition. We used Affymetrix microarrays to analyze host cell transcription after pre-treatment with the protein synthesis inhibitor cyclohexamide (CHX), Toxoplasma infection, and subsequent interferon-gamma stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34916 | GEO | 2015/08/01

SECONDARY ACCESSION(S): PRJNA150163

REPOSITORIES: GEO

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Expression data from cyclohexamide treated Human Foreskin Fibroblasts (HFFs) infected with type I Toxoplasma gondii and stimulated with interferon gamma.

Project description:Pre-infection with Toxoplasma parasites inhibits induction of an interferon gamma responsive gene expression program. In this study we aimed to determine what role host negative regulatory proteins that are induced by Toxoplasma infection, such as SOCS-1, have in this inhibition. We used Affymetrix microarrays to analyze host cell transcription after pre-treatment with the protein synthesis inhibitor cyclohexamide (CHX), Toxoplasma infection, and subsequent interferon-gamma stimulation. Human foreskin fibroblasts (HFFs) were left untreated or treated with CHX for 40min. Cells were infected, or not, with type I (RH) Toxoplasma parasites, for one hour, and subsequently stimulated with human IFN-γ for one hour. Total RNA was isolated and hybridized to Affymetrix Human U133A 2.0 gene chips.

2015-08-01 | E-GEOD-34916 | biostudies-arrayexpress

Expression data from human foreskin fibroblasts (HFFs) infected with Toxoplasma gondii

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Expression data from Human foreskin fibroblasts (HFFs) infected with Toxoplasma gondii.

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Expression data from RAW264.7 murine macrophages infected with Toxoplasma gondii and subsequently stimulated with interferon-gamma

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Expression data from RAW264.7 murine macrophages infected with Toxoplasma gondii and subsequently stimulated with interferon-gamma

Project description:Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe). We used Affymetrix microarrays to analyze host cell transcription after Toxoplasma infection and interferon-gamma stimulation. RAW264.7 murine macrophages were left uninfected or infected with type I (RH), type I ?rop16 (RH ?rop16), type II (Pru), type II ?gra15 (Pru ?gra15), or type II (CEP) parasites at an MOI ~5 for 18 hours and subsequently stimulated with murine IFN-? for six hours. Plaque assays were done to assess parasite viability. Total RNA was isolated and hybridized to Affymetrix Mouse 430A 2.0 gene chips.

2013-02-19 | E-GEOD-34913 | biostudies-arrayexpress

Effect of Toxoplasma gondii efector TgIST on global transcriptome of human foreskin fibroblasts (HFFs) upon type I IFN activation

Project description:TgIST is an effector secreted by Toxoplasma gondii into the host cell that translocates to the nucleus and block STAT1 mediated transcription. STAT1 is involved in type I and II interferon (IFN) mediated upregulation of range of anti-parasitic molecules. A total of 544,234,059 read sequences generated from 3 independent biological replicates were mapped to human hg19 reference genome. Type I IFN activation of HFFs infected with TgIST knockout parasites showed upregulation of genes involved in interferon signaling compared to wild type parasites.

2019-06-30 | GSE125066 | GEO

Expression data from Human foreskin fibroblasts (HFFs) infected with Toxoplasma gondii.

Project description:Toxoplasma strains have been shown to modulate host cell transcription. We have found a type II Toxoplasma gene, GRA15, which activates the nuclear translocation of the NF-kappaB p65 transcription factor. We used microarrays to determine how GRA15II modulates host cell transcription. HFFs were infected with type I (RH), type I GRA15II (RH GRA15II), type II (Pru), type II GRA15KO (Pru GRA15KO), type III (cep), or type III GRA15II (cep GRA15II) parasites for 18-24 hours. Some samples were also stimulated with TNF-alpha. Total RNA was isolated and hybridized to Affymetrix GeneChip Human Genome U133A 2.0 arrays.

2011-01-10 | E-GEOD-25468 | biostudies-arrayexpress

Expression data from human foreskin fibroblasts (HFFs) infected with type I strains of Toxoplasma gondii.

2013-08-20 | GSE44189 | 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

Expression data from human foreskin fibroblasts (HFFs) infected with type I strains of Toxoplasma gondii.

Project description:Type I strains of Toxoplasma gondii exhibit phenotypic variation, but it is uncertain how differently type I strains modulate the host cell. We determined differential host modulation by type I strains through microarray. HFFs were infected with RH-ERP, RH-JSR and GT1 for 24 hours. Total RNA was isolated and hybridized to Affymetrix GeneChip Human Genome U133A 2.0 arrays.

2013-08-20 | E-GEOD-44189 | biostudies-arrayexpress

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