Mus musculus
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ABSTRACT:
PROVIDER: PRJNA189456 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Virulent Francisella tularensis induces a unique pulmonary inflammatory response characterized by temporal regulation of innate immune pathways correlating with altered bacterial gene expression patterns.
2013-04-15 | GSE44320 | GEO
Project description:Virulent Francisella tularensis induces a unique pulmonary inflammatory response characterized by temporal regulation of innate immune pathways correlating with altered bacterial gene expression patterns. The pulmonary transcriptional response to aerosolized virulent F. tularensis was compared to other lethal and non-lethal respiratory pathogens.
2013-04-15 | E-GEOD-44320 | biostudies-arrayexpress
Project description:Francisella tularensis is a category A select agent based on its infectivity and virulence but disease mechanisms in F. tularensis infection remain poorly understood. A murine pulmonary model of infection was therefore employed to characterize the host immune response to F. tularensis infection and to discern differences in responses to infection with the highly virulent Type A F. tularensis strain Schu4 and to the less virulent Type B live vaccine strain (LVS). Mice were infected intranasally with F. tularensis Schu4 or LVS and organ lesions were assessed 48 and 120 hours after infection. Experiments were also conducted to assess and compare the host immune response to infection using global transcriptional analysis. Mice were infected via low dose aerosol with F. tularensis Schu4 or LVS strains, and transcriptional response in the lungs and spleen was monitored using full mouse genome microarrays at 12, 24, 48, and 120 hours after infection. We found differential and temporal differences in expression of cytokine and chemokine genes, CD molecules, apoptosis, leukocytes and adhesion receptors, and immunological signaling between infection with Schu4 and LVS strains. The transcriptional differences coincided with marked differences in the timing and extent of organ lesions in mice infected with the LVS and Schu4 strains. Thus, these studies revealed both temporal and qualitative differences in the host immune response to infection with virulent F. tularensis Schu4 compared to infection with LVS.
2010-11-01 | GSE22203 | GEO
Project description:Francisella tularensis is a category A select agent based on its infectivity and virulence but disease mechanisms in F. tularensis infection remain poorly understood. A murine pulmonary model of infection was therefore employed to characterize the host immune response to F. tularensis infection and to discern differences in responses to infection with the highly virulent Type A F. tularensis strain Schu4 and to the less virulent Type B live vaccine strain (LVS). Mice were infected intranasally with F. tularensis Schu4 or LVS and organ lesions were assessed 48 and 120 hours after infection. Experiments were also conducted to assess and compare the host immune response to infection using global transcriptional analysis. Mice were infected via low dose aerosol with F. tularensis Schu4 or LVS strains, and transcriptional response in the lungs and spleen was monitored using full mouse genome microarrays at 12, 24, 48, and 120 hours after infection. We found differential and temporal differences in expression of cytokine and chemokine genes, CD molecules, apoptosis, leukocytes and adhesion receptors, and immunological signaling between infection with Schu4 and LVS strains. The transcriptional differences coincided with marked differences in the timing and extent of organ lesions in mice infected with the LVS and Schu4 strains. Thus, these studies revealed both temporal and qualitative differences in the host immune response to infection with virulent F. tularensis Schu4 compared to infection with LVS. 18 mice total, 2 uninfected controls, 2 mice per time point, time points were 12 hour/24 hour/48 hour/ 120 hour post infection, 2 infection groups: LVS and Schu4 infection. Lung and spleen were harvested at each time point, poly A RNA was extracted, converted to cDNA, labeled and hybridized in triplicate
2010-11-01 | E-GEOD-22203 | biostudies-arrayexpress
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.
This model is hosted on
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MODEL1507180003.
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2015-07-30 | MODEL1507180003 | BioModels
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: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. Six groups of 4 mice were exposed to aerosolised Francisella tularensis and a three groups exposed to vehicle only control (media only). Following exposure mice were culled at 4 timepoints (1, 24, 48 and 96h). RNA was extracted and run on the custom array.
2011-03-01 | E-GEOD-17248 | biostudies-arrayexpress
Project description:Francisella are pathogenic bacteria whose virulence is linked to their ability to replicate within the host cell cytosol. Entry into the macrophage cytosol activates a host protective multimolecular complex called the inflammasome to release the proinflammatory cytokines IL-1 and IL-18 and trigger caspase-1 dependent cell death. Here we show that cytosolic Francisella induce a type I interferon (IFN) response that is essential for caspase-1 activation, inflammasome mediated cell death, and release of IL-1 and IL-18. Extensive type I IFN dependent cell death resulting in macrophage depletion occurs in vivo during Francisella infection. Type I IFN is also necessary for inflammasome activation in response to cytosolic Listeria but not vacuole localized Salmonella or extracellular ATP. These results show the specific connection between type I IFN signaling and inflammasome activation, two sequential events triggered by recognition of cytosolic bacteria. To our knowledge, this is the first example of positive regulation of inflammasome activation. This connection underscores the importance of cytosolic recognition of pathogens and highlights how multiple innate immunity pathways interact before commitment to critical host responses. Keywords: murine macrophage response to Francisella tularensis subspecies novicida infection We analyzed a series of 18 MEEBO arrays on which were hybed RNA randomly amplified from bone marrow derived macrophages infected or not with WT Francisella tularensis subspecies novicida or a the mglA mutant strain GB2.
2007-05-23 | E-GEOD-7684 | biostudies-arrayexpress
Project description:Ubiquitination/deubiquitination belong to the most important regulatory mechanisms carried out through the attachment/removal of the ubiquitin molecule, respectively. The process is necessary not only to mark molecules for degradation, but also for example to the activation of signaling pathways leading to pro-inflammatory host response. Many intracellular pathogens, such as Francisella tularensis, have evolved mechanisms of blocking such host immune responses to escape degradation. Here, we describe that F. tularensis interferes with the host's ubiquitination system. We showed increased total activity of deubiquitinating enzymes (DUBs) in human macrophages after infection and confirmed the reduced enzymatic activities of two specific DUBs: USP10 and UCH-L5, and the increased activity of USP25. We further revealed the enrichment of these three enzymes in exosomes derived from F. tularensis-infected cells.
2023-10-24 | PXD043492 | Pride