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Anthrax Lethal Toxin-Inducd Gene Expression Changes in Mouse Lung

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE28554 | GEO | 2011/09/07

SECONDARY ACCESSION(S): PRJNA139069

REPOSITORIES: GEO

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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

Expression data from anthrax lethal toxin treated primary cardiomyocytes from 1-3-day-old neonatal Balb/c mice

Project description:The activity of known anthrax lethal toxin is insufficient to account the effects on functions of cardiomyocytes. In vivo and in vitro studies showed that Anthrax lethal toxin (LeTx) induce 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.

2018-07-07 | GSE116755 | GEO

RNA Sequencing Reveals Immunosuppressive Role of Anthrax Lethal Toxin in Human Lung Epithelial and Monocytic Cells

Project description:Using RNA-seq, we report here that anthrax lethal toxin (LeTx) induces immunosuppression in human lung epithelial cell line A549 and monocytic cell line U937.

2017-01-26 | GSE77219 | 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

Bacillus anthracis' lethal toxin induces broad transcriptional responses in human peripheral monocyte.

Project description:Anthrax lethal toxin directly targets human peripheral monocytes and causes multiple aberrant gene responses that would be expected to result in defects in human monocyte’s normal signaling transduction pathways and nction. This study provides further insights into the mechanisms associated with the host immune system collapse during an anthrax infection, and suggests that anthrax LT may have additional targets outside the well-known MAPK pathway.

2012-12-12 | GSE34407 | GEO

Bacillus anthracis' lethal toxin induces broad transcriptional responses in human peripheral monocyte.

Project description:Anthrax lethal toxin directly targets human peripheral monocytes and causes multiple aberrant gene responses that would be expected to result in defects in human monocyteM-bM-^@M-^Ys normal signaling transduction pathways and nction. This study provides further insights into the mechanisms associated with the host immune system collapse during an anthrax infection, and suggests that anthrax LT may have additional targets outside the well-known MAPK pathway. There were 4 replicates, 1 control and 1 toxin treated from 4 donors, with 8 samples total. key word : Toxin response

2012-12-12 | E-GEOD-34407 | biostudies-arrayexpress

Anthrax toxin receptor 2-dependent lethal toxin killing in vivo.

Project description:Anthrax toxin receptors 1 and 2 (ANTXR1 and ANTXR2) have a related integrin-like inserted (I) domain which interacts with a metal cation that is coordinated by residue D683 of the protective antigen (PA) subunit of anthrax toxin. The receptor-bound metal ion and PA residue D683 are critical for ANTXR1-PA binding. Since PA can bind to ANTXR2 with reduced affinity in the absence of metal ions, we reasoned that D683 mutant forms of PA might specifically interact with ANTXR2. We show here that this is the case. The differential ability of ANTXR1 and ANTXR2 to bind D683 mutant PA proteins was mapped to nonconserved receptor residues at the binding interface with PA domain 2. Moreover, a D683K mutant form of PA that bound specifically to human and rat ANTXR2 mediated killing of rats by anthrax lethal toxin, providing strong evidence for the physiological importance of ANTXR2 in anthrax disease pathogenesis.

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

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. Keywords: Time course

2007-09-28 | GSE9184 | GEO

Suppressive effects of anthrax lethal toxin on megakaryopoiesis.

Project description:Anthrax lethal toxin (LT) is a major virulence factor of Bacillus anthracis. LT challenge suppresses platelet counts and platelet function in mice, however, the mechanism responsible for thrombocytopenia remains unclear. LT inhibits cellular mitogen-activated protein kinases (MAPKs), which are vital pathways responsible for cell survival, differentiation, and maturation. One of the MAPKs, the MEK1/2-extracellular signal-regulated kinase pathway, is particularly important in megakaryopoiesis. This study evaluates the hypothesis that LT may suppress the progenitor cells of platelets, thereby inducing thrombocytopenic responses. Using cord blood-derived CD34(+) cells and mouse bone marrow mononuclear cells to perform in vitro differentiation, this work shows that LT suppresses megakaryopoiesis by reducing the survival of megakaryocytes. Thrombopoietin treatments can reduce thrombocytopenia, megakaryocytic suppression, and the quick onset of lethality in LT-challenged mice. These results suggest that megakaryocytic suppression is one of the mechanisms by which LT induces thrombocytopenia. These findings may provide new insights for developing feasible approaches against anthrax.

| S-EPMC3605335 | biostudies-other

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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