Lung transcriptome from M. avium infected WT, IFNg-/- and IRF1-/- mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE11809 | GEO | 2008/09/01
SECONDARY ACCESSION(S): PRJNA105897
REPOSITORIES: GEO
Similar Datasets
Project description:Mycobacterium avium infection in mice induces granuloma necrosis in the lung which is dependent on IFNg. IRF1 is a transcription factor activated by IFNg signaling. The effect of IFNg and IRF1 on immunopathology and transcriptional changes in the lung were analysed using gene-deficient mice. The data from the Ifng-/- experiment have been described (Aly et al. 2007. J Pathol 212:295). Experiment Overall Design: In two independent blocks of experiments, Ifng-/- and Irf1-/- mice on a C57Bl/6 background and their respective controls were infected with Mycobacterium avium via aerosol. After 14 weeks, mice were sacrificed and the lung RNA prepared using TriFast FL (Peqlab). Total RNA (1µg) was labeled and hybridized to Affymetrix mouse MOE430A 2.0 GeneChips according to the manufacturerâs recommendations. For each condition three biological replicates (except Ifng-/-, no infection) were used. Total of 23 Samples.
2008-10-25 | E-GEOD-11809 | biostudies-arrayexpress
Project description:This experiment was designed to identify IFNg-regulated, IRF1-dependent genes during infection with the intracellular pathogen Shigella flexneri. WT and Irf1-/- MEFs were stimulated for 18 hours with IFNg or left unstimulated; all of the cells were subsequently infected for 6 hours with S. flexneri prior to harvest of total RNA.
2011-09-01 | E-MTAB-713 | biostudies-arrayexpress
Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 16MB gene locus(HG17) Keywords: ChIP-chip three replicates for each marker at each state.
2009-01-14 | E-GEOD-11131 | biostudies-arrayexpress
Project description:Mycobacterium avium subspecies paratuberculosis (MAP) infection is established following the ingestion of bacteria, their penetration of the intestinal mucosa and subsequent events of the host-parasite interaction. These bacteria invade M cells, macrophages and are capable of resisting host defenses and multiply to reach very high numbers intracellular. Mycobactrium avium subsp. avium (MAA) is an antigenically and genetically similar organisms but is relatively nonpathogenic for cattle. MAA organisms appear to infect cattle, but unlike cattle infected with MAP, cattle infected with MAA typically mount an effective systemic immune response, form caseous granuloma, and eliminate the infection. This study was designed to understand the similarities and differences in the host responses during MAP and MAA infection. Neonatal calves were infected (ligated ileal loops) with PBS, MAP, or avirulent MAA following which samples were collected at 30 min, 1h, 2h, 4h, 8h, or 12h. Post-infection, RNA was collected, processed, and then hybridized to custom bovine gene expression arrays, each of which represented 13,258 transcripts spotted in duplicate. Arrays were normalized by scaling against the average reference intensity value (i.e., average across all arrays), normalized by global mean, and then log transformed before statistical analyses were performed. Pairwise comparisons of averaged signal values and Student’s t test were performed using GeneSifter software (VizX Labs, Seattle, WA). A fold-change of at least 1.5-fold and a p value of 0.05 or less was required for a difference in signal to be considered statistically significant. When comparing the transcriptional responses of calves infected with the MAA versus MAP, unique patterns of expression were clearly visible. In general, numbers of transcripts altered in response to infection were much greater for MAA-infected animals than for those infected with the MAP. No genes were significantly up-regulated in MAP-infected animals at the earliest time point tested (30 min), and only modest numbers of genes were increased in expression over the experimental time course. On the other hand, up-regulated transcripts were detected by 30 min in MAA-infected animals and peaked by 2 hr. Differences in the numbers of down-regulated genes between MAP-infected and MAA-infected animals (compared to PBS-infected controls) were less pronounced. At the earliest time points, MAP-infected calves had a greater number of down-regulated genes than did animals infected with MAA. This trend was reversed at 8 and 12 hr post-infection. Keywords: Gene expression profiling by microarray
2012-10-03 | GSE13888 | GEO
Project description:Analysis of STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucleotide probes at 30bp intervals tiling over non-repetitive 16MB gene locus (HG17).
2017-12-22 | GSE94352 | GEO
Project description:Mycobacterium avium subspecies paratuberculosis (MAP) infection is established following the ingestion of bacteria, their penetration of the intestinal mucosa and subsequent events of the host-parasite interaction. These bacteria invade M cells, macrophages and are capable of resisting host defenses and multiply to reach very high numbers intracellular. Mycobactrium avium subsp. avium (MAA) is an antigenically and genetically similar organisms but is relatively nonpathogenic for cattle. MAA organisms appear to infect cattle, but unlike cattle infected with MAP, cattle infected with MAA typically mount an effective systemic immune response, form caseous granuloma, and eliminate the infection. This study was designed to understand the similarities and differences in the host responses during MAP and MAA infection. Neonatal calves were infected (ligated ileal loops) with PBS, MAP, or avirulent MAA following which samples were collected at 30 min, 1h, 2h, 4h, 8h, or 12h. Post-infection, RNA was collected, processed, and then hybridized to custom bovine gene expression arrays, each of which represented 13,258 transcripts spotted in duplicate. Arrays were normalized by scaling against the average reference intensity value (i.e., average across all arrays), normalized by global mean, and then log transformed before statistical analyses were performed. Pairwise comparisons of averaged signal values and StudentM-bM-^@M-^Ys t test were performed using GeneSifter software (VizX Labs, Seattle, WA). A fold-change of at least 1.5-fold and a p value of 0.05 or less was required for a difference in signal to be considered statistically significant. When comparing the transcriptional responses of calves infected with the MAA versus MAP, unique patterns of expression were clearly visible. In general, numbers of transcripts altered in response to infection were much greater for MAA-infected animals than for those infected with the MAP. No genes were significantly up-regulated in MAP-infected animals at the earliest time point tested (30 min), and only modest numbers of genes were increased in expression over the experimental time course. On the other hand, up-regulated transcripts were detected by 30 min in MAA-infected animals and peaked by 2 hr. Differences in the numbers of down-regulated genes between MAP-infected and MAA-infected animals (compared to PBS-infected controls) were less pronounced. At the earliest time points, MAP-infected calves had a greater number of down-regulated genes than did animals infected with MAA. This trend was reversed at 8 and 12 hr post-infection. Keywords: Gene expression profiling by microarray Microarrays were used to examine the transcriptional profiles of bovine intestinal mucosa inoculated with PBS, MAP or MAA and across six time points (30 min, 1, 2, 4, 8, and 12 hours). Experiments were performed in quadruplicate for PBS, MAP, and MAA (bovine ligated ileal loops surgeries were performed with four calves). For one surgery, MAA was used for 4 time ponts only, thus generateing a total of 70 arrays.
2012-10-03 | E-GEOD-13888 | biostudies-arrayexpress
Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 16MB gene locus(HG17) Keywords: ChIP-chip
2009-01-15 | GSE11131 | GEO
Project description:Lung transcriptome from M. avium infected WT, IFNg-/- and IRF1-/- mice
| PRJNA105897 | ENA
Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 122kb CIITA locus(HG17) Keywords: ChIP-chip
2008-04-15 | GSE10206 | GEO
Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).
2014-11-13 | E-GEOD-49469 | biostudies-arrayexpress