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Expression profile from anthrax edema toxin (ET) treated murine bone marrow derived macrophages (BMDM)

ABSTRACT: Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Keywords: Time course

ORGANISM(S): Mus musculus

PROVIDER: GSE9184 | GEO | 2007/09/28

SECONDARY ACCESSION(S): PRJNA102751

REPOSITORIES: GEO

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Transcription profiling of mouse bone marrow derived macrophages (BMDM) treated with anthrax edema toxin (ET)

Project description:Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Experiment Overall Design: BMDM were treated with 1 mg/ml of ET and the RNAs were purified at 0, 2, and 4h after toxin treatment.

2008-06-16 | E-GEOD-9184 | biostudies-arrayexpress

Edema Toxin-treated Macrophage Study

2006-10-24 | GSE4712 | GEO

HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT) Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment.

2009-08-25 | GSE17777 | GEO

Transcription profiling of murine macrophage-like RAW 264.7 cells treated with EdTx, protective antigen, or LPS for different length of time to examine the effect of EdTx on global transcriptional profiles.

Project description:Edema toxin (EdTx), which is a combination of edema factor and a binding moiety (protective antigen), is produced by Bacillus anthracis, the etiological agent of anthrax. EdTx is an adenylyl cyclase enzyme that converts adenosine triphosphate to adenosine-3',5'-monophosphate, resulting in interstitial edema seen in anthrax patients. We used GeneChip analysis to examine global transcriptional profiles of EdTx-treated RAW 264.7 murine macrophage-like cells at 3 and 6 hr. Experiment Overall Design: RAW 264.7 cells were treated with EdTx (2.5 µg/ml of protective antigen and 0.625 µg/ml of Edema factor), PA (2.5 µg/ml), or LPS (1 ng/mL) for 0, 3, and 6 hr. Each experiment was performed in triplicate, generating a total of 21 arrays (biological replciates).

2007-11-22 | E-GEOD-4712 | biostudies-arrayexpress

Anthrax toxins regulate pain signaling and can deliver molecular cargoes to Antxr2+ DRG sensory neurons

Project description:We found that intrathecal injection of anthrax edema toxin (ET), causes analgesia in adult B6J mice. In order to determine if DRG neuron transcriptional responses play a role in pain blockade, we performed a bulk RNA-seq experiment on dissected mouse DRG neurons. We report that anthrax edema toxin causes transcriptional responses in DRG neurons 2h after in vivo administration

2021-09-29 | GSE184619 | GEO

Transcription profiling of human HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT); Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.

2009-09-13 | E-GEOD-17777 | biostudies-arrayexpress

Expression data from edema toxin treated primary hepatocytes from 1–3-day-old neonatal A/J mice

Project description:The activity of known anthrax toxins is insufficient to account the effects on functions of hepatocytes. In vivo and in vitro studies showed that Anthrax edema toxin (EdTx) induce lethal liver and heart damage We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process.

2018-06-16 | GSE115844 | GEO

Multiple stages of evolutionary change in anthrax toxin receptor expression in humans

Project description:The advent of animal husbandry and hunting increased human exposure to zoonotic pathogens. To understand how a zoonotic disease influenced human evolution, we studied changes in human expression of anthrax toxin receptor 2 (ANTXR2), which encodes a cell surface protein necessary for Bacillus anthracis virulence toxins to cause anthrax disease. In immune cells, ANTXR2 was 8-fold down-regulated in all available human samples compared to non-human primates, indicating regulatory changes early in the evolution of modern humans. We also observed multiple genetic signatures consistent with recent positive selection driving a European-specific decrease in ANTXR2 expression in several non-immune tissues affected by anthrax toxins. Our observations fit a model in which humans adapted to anthrax disease following early ecological changes associated with hunting and scavenging, as well as a second period of adaptation after the rise of modern agriculture.

2020-08-14 | GSE156161 | GEO

Anthrax Lethal Toxin-Inducd Gene Expression Changes in Mouse Lung

Project description:Enhanced susceptibility of A/J mice to death by systemic anthrax lethal toxin (LeTx) administration compared to the C57BL/6 strain was observed. In this study we investigated whether systemic exposure of mice to LeTx would induce gene expression changes associated with vascular/capillary leakage in lung tissue. Lungs of the less susceptible C57BL/6 strain showed 80% fewer differentially expressed genes compared to lungs of the more sensitive A/J strain. Total RNA obtained from lung tissue of C57Bl/6 and A/J strain mice exposed for 6 and 12 hrs to wild-type and mutant Bacillus anthracis.

2011-09-06 | E-GEOD-28554 | biostudies-arrayexpress

Discovery of Mouse Spleen Signaling Responses to Anthrax using Label-Free Quantitative Phosphoproteomics via Mass Spectrometry

Project description:From article abstract: Inhalational anthrax is caused by spores of the bacterium Bacillus anthracis (B. anthracis), and is an extremely dangerous disease that can kill unvaccinated victims within 2 weeks. Modern antibiotic-based therapy can increase the survival rate to ~50%, but only if administered presymptomatically (within 24-48 h of exposure). To discover host signaling responses to presymptomatic anthrax, label-free quantitative phosphoproteomics via liquid chromatography coupled to mass spectrometry was used to compare spleens from uninfected and spore-challenged mice over a 72 h time-course. Late-stage (48-72 h post-challenge) Sterne strain (lethal) infections resulted in global alterations to the spleen phosphoproteome. In contrast, delta-Sterne strain (asymptomatic; missing the anthrax toxin) infections resulted in 188 (5.8%) significantly altered (q<0.05) phosphopeptides. Twenty-six highly tentative phosphorylation responses to early-stage (24 h post-challenge) anthrax were discovered (q<0.5), and ten of these originated from eight proteins that have known roles in the host immune response. These tentative early-anthrax host response signaling events within mouse spleens may translate into presymptomatic diagnostic biomarkers of human anthrax detectable within circulating immune cells, and could aid in the identification of pathogenic mechanisms and therapeutic targets. [Molecular & Cellular Proteomics 10: 10.1074/mcp.M110.000927, 1–11, 2011. The files in this dataset are exactly the same files that were originally uploaded to Proteome Commons Tranche as described in the article.]

2017-03-22 | PXD006148 | Pride

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