Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-12108
PROVIDER: PRJNA113801 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Differential expression in human peripheral blood monocytes between F. novicida-infected and uninfected, and between Francisella tularensis tularensis isolate Schu S4 and uninfected. The goal was to examine genomewide transcriptional reponses to these two strains, and identify differentially-regulated genes that may help explain the virulence of Schu S4. Keywords: Immune Response, Human Monocytes, Bacteria, Francisella
2008-08-13 | GSE12108 | GEO
Project description:Differential expression in human peripheral blood monocytes between F. novicida-infected and uninfected, and between Francisella tularensis tularensis isolate Schu S4 and uninfected. The goal was to examine genomewide transcriptional reponses to these two strains, and identify differentially-regulated genes that may help explain the virulence of Schu S4. Experiment Overall Design: Human monocytes were infected with the Schu S4 isolate of Francisella tularensis tularensis (n=4), with F. tularensis subspecies novicida isolate U112 (n=4) or were left uninfected (n=6). Gene expression values were calculated using the gcrma package in R and BioConductor, and limma to identify differentially expressed genes. Submitted here are expression values calculated using R 2.7.1 and BioConductor 2.2 (FreeBSD/amd64) but the original were done using R 2.6.1 and BioConductor 2.1 (FreeBSD/amd64). Twelve other chips were pooled with these 14 for preprocessing.
2008-10-25 | E-GEOD-12108 | biostudies-arrayexpress
Project description:We demonstrated recently that both constitutive and FAS-triggered apoptosis of human neutrophils are profoundly impaired by Francisella tularensis, but how this is achieved is largely unknown. To test the hypothesis that changes in neutrophil gene expression contribute to this phenotype, we used human oligonucleotide microarrays to identify differentially regulated genes in cells infected with F. tularensis strain LVS compared with uninfected controls. In order to examine the effect of F. tularensis on the neutrophil transcriptome, we performed microarray expression analysis on human neutrophils treated with F. tularensis subsp. holarctica live vaccine strain (LVS).
2012-10-22 | GSE37416 | GEO
Project description:Francisella tularensis is a Gram-negative bacterium that causes a fatal human disease known as tularemia. The Centers for Disease Control have classified F. tularensis as Category A Tier-1 Select Agent. The virulence mechanisms of Francisella are not entirely understood. Francisella possesses very few transcription regulators, and most of these regulate the expression of genes involved in intracellular survival and virulence. The F. tularensis genome sequence analysis reveals an AraC (FTL_0689) transcriptional regulator homologous to the AraC/XylS family of transcriptional regulators. In Gram-negative bacteria, AraC activates genes required for L-arabinose utilization and catabolism. The role of the FTL_0689 regulator in F. tularensis is not known. In this study, we characterized the role of FTL_0689 in gene regulation of F. tularensis and investigated its contribution to intracellular survival and virulence. The results demonstrate that FTL_0689 in Francisella is not required for L-arabinose utilization. Instead, FTL_0689 specifically regulates the expression of the oxidative and global stress response, virulence, metabolism, and other key pathways genes required by Francisella when exposed to oxidative stress. The FTL_0689 mutant is attenuated for intramacrophage growth, and mice infected with the FTL_0689 mutant survive better than wild-type F. tularensis LVS infected mice. Based on the deletion mutant phenotype, FTL_0689 was termed osrR (oxidative stress response regulator). Altogether, this study elucidates the role of the osrR transcriptional regulator in tularemia pathogenesis.
2021-10-13 | GSE183001 | GEO
Project description:We wanted to identify Francisella tularensis bacterial mutants that are negatively selected in vivo in the lungs of mice. Mice were infected with a Francisella transposon mutant library where each gene in the genome has been mutated via the insertion of a kanamycin resistance cassette with 2 outward facing T7 promoters. 2 days post infection, infected lungs were harvested and the bacteria present in the infected lungs were collected. Bacterial genomic DNA was isolated and subjected to an in vitro T7 transcription reaction, reverse transcribed and the resulting cDNA was hybridized to our Francisella microarray. Infection: The goal of the study was to identify Francisella genes that are negatively selected in the lungs of mice post infection with a Francisella transposon mutant library. Resulting bacterial cDNA was hybridized to the Francisella microarray.
2010-06-09 | GSE22231 | GEO
Project description:The goal of this study is to determine the host response of human epithelial cells during infection with Francisella Tularensis. For this purpose, A549 human epithelial cell line was infected with Francisella tularensis spp. holarctica strain LVS for different times of infection, in duplicates. At different times post infection (0.5/1/3/6/12/24 hours post infection) cells were harvested and total RNA was extracted. RNA-seq libraries were constructed and sequencing of 100bp paired-end was performed on the Illumina NovaSeq 6000 system. Sequencing yielded about 22M reads per sample that were mapped to the human genome (Human: GRCh38) resulting with the identification of 21,066 transcripts. The expression of the infected samples was compared to mock sample, and RNA ratios were clustered using partitioning clustering. This approach allowed clustering of the cellular transcripts into 5 distinct classes based on similarities in temporal expression profiles. We next carried out GO term enrichment analysis for each of these five cluster. Our study represents the first detailed analysis of human epithelial response to Francisella tularensis infection, and provide a framework for comparative investigations of genes and mechanisms that may contribute to the infection.
2020-08-11 | GSE155970 | GEO
Project description:We demonstrated recently that both constitutive and FAS-triggered apoptosis of human neutrophils are profoundly impaired by Francisella tularensis, but how this is achieved is largely unknown. To test the hypothesis that changes in neutrophil gene expression contribute to this phenotype, we used human oligonucleotide microarrays to identify differentially regulated genes in cells infected with F. tularensis strain LVS compared with uninfected controls. In order to examine the effect of F. tularensis on the neutrophil transcriptome, we performed microarray expression analysis on human neutrophils treated with F. tularensis subsp. holarctica live vaccine strain (LVS). Polymorphonuclear leukocytes (PMNs) were isolated from the blood of healthy donors. Control and F. tularensis-exposed PMNs were incubated at 37C for 0, 3, 6, 12, 24, and 48 hours.
2012-10-22 | E-GEOD-37416 | biostudies-arrayexpress
Project description:The microarray analysis of Francisella tularensis subsp. tularensis strains SCHU P9 (virulent) and SCHU P0/P5 (attenuated) revealed significant differences in gene expression. The results showed that 19 genes were upregulated in the virulent SCHU P9 strain, while two genes, including ftt_0965c, were significantly downregulated
2024-12-31 | GSE274776 | GEO
Project description:Francisella tularensis may enter the body thorugh the lungs and cause fatal infection. In this study the inflammatory response to the virulent strain of Francisella (Schu4) was mapped over a 96h time-course using a custom microarray.
2011-03-01 | GSE17248 | GEO
Project description:Raghunathan2010 - Genome-scale metabolic
network of Francisella tularensis (iRS605)
This model is described in the article:
Systems approach to
investigating host-pathogen interactions in infections with the
biothreat agent Francisella. Constraints-based model of
Francisella tularensis.
Raghunathan A, Shin S, Daefler
S.
BMC Syst Biol 2010; 4: 118
Abstract:
BACKGROUND: Francisella tularensis is a prototypic example
of a pathogen for which few experimental datasets exist, but
for which copious high-throughout data are becoming available
because of its re-emerging significance as biothreat agent. The
virulence of Francisella tularensis depends on its growth
capabilities within a defined environmental niche of the host
cell. RESULTS: We reconstructed the metabolism of Francisella
as a stoichiometric matrix. This systems biology approach
demonstrated that changes in carbohydrate utilization and amino
acid metabolism play a pivotal role in growth, acid resistance,
and energy homeostasis during infection with Francisella. We
also show how varying the expression of certain metabolic genes
in different environments efficiently controls the metabolic
capacity of F. tularensis. Selective gene-expression analysis
showed modulation of sugar catabolism by switching from
oxidative metabolism (TCA cycle) in the initial stages of
infection to fatty acid oxidation and gluconeogenesis later on.
Computational analysis with constraints derived from
experimental data revealed a limited set of metabolic genes
that are operational during infection. CONCLUSIONS: This
integrated systems approach provides an important tool to
understand the pathogenesis of an ill-characterized biothreat
agent and to identify potential novel drug targets when rapid
target identification is required should such microbes be
intentionally released or become epidemic.
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2015-07-30 | MODEL1507180003 | BioModels