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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34407 | GEO | 2012/12/12

SECONDARY ACCESSION(S): PRJNA149645

REPOSITORIES: GEO

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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

Transcription profiling of human NB4 cells treated with lethal Bacillus anthracis toxin

Project description:Bacillus anthracis lethal toxin (LT) exposure on NB-4 cells Experiment Overall Design: color-swap dye-reversal

2008-06-14 | E-GEOD-5966 | biostudies-arrayexpress

Transcriptome of Bacillus anthracis lethal toxin (LT)-intoxicated HUVECs monolayers

Project description:We have analyzed the variation of transcriptome of HUVECs intoxicated by the lethal toxin of Bacillus anthracis at 4 and 8 hours

2010-01-26 | GSE12131 | GEO

NB4 cells treated with lethal toxin

Project description:Bacillus anthracis lethal toxin (LT) exposure on NB-4 cells Keywords: time course

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

Project description:Anthrax lethal toxin (LT), produced by the Gram-positive bacterium Bacillus anthracis, is a highly effective zinc dependent metalloprotease that cleaves the N-terminus of mitogen-activated protein kinase kinases (MAPKK or MEKs) and is known to play a role in impairing the host immune system during an inhalation anthrax infection. Here, we present the transcriptional responses of LT treated human monocytes in order to further elucidate the mechanisms of LT inhibition on the host immune system.Western Blot analysis demonstrated cleavage of endogenous MEK1 and MEK3 when human monocytes were treated with 500 ng/mL LT for four hours, proving their susceptibility to anthrax lethal toxin. Furthermore, staining with annexin V and propidium iodide revealed that LT treatment did not induce human peripheral monocyte apoptosis or necrosis. Using Affymetrix Human Genome U133 Plus 2.0 Arrays, we identified over 820 probe sets differentially regulated after LT treatment at the p <0.001 significance level, interrupting the normal transduction of over 60 known pathways. As expected, the MAPKK signaling pathway was most drastically affected by LT, but numerous genes outside the well-recognized pathways were also influenced by LT including the IL-18 signaling pathway, Toll-like receptor pathway and the IFN alpha signaling pathway. Multiple genes involved in actin regulation, signal transduction, transcriptional regulation and cytokine signaling were identified after treatment with anthrax LT.We conclude LT directly targets human peripheral monocytes and causes multiple aberrant gene responses that would be expected to be associated with defects in human monocyte's normal signaling transduction pathways and function. 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 downstream targets outside the well-known MAPK pathway.

| S-EPMC3475123 | biostudies-literature

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

Transcription profiling of human cells treated with Bacillus anthracis lethal toxin (LT)-intoxicated HUVECs monolayers

Project description:We have analyzed the variation of transcriptome of HUVECs intoxicated by the lethal toxin of Bacillus anthracis at 4 and 8 hours Experiment Overall Design: Three experimental conditions with two biological replicates for the control condition corresponding to untreated HUVEC monolayer. RNA were extracted before labeling and hybridizations on Human U133A Plus 2.0 Affymetrix GeneChip

2010-01-29 | E-GEOD-12131 | biostudies-arrayexpress

Toxin-induced resistance in Bacillus anthracis lethal toxin-treated macrophages.

Project description:In the current study, we show that macrophages adaptively resist anthrax lethal toxin (LT) through a toxin-activated process termed toxin-induced resistance (TIR). TIR was triggered by pretreatment of RAW 264.7 or J774A.1 macrophages with a low dose of LT for at least 6 h, which resulted in resistance to high doses of LT for 96 h. Activation of TIR required functional toxin, because LT subunits, mutants, and heat-inactivated toxin were unable to trigger resistance. TIR macrophages were not altered in toxin receptor levels or cell cycle profiles. Treatment of TIR macrophages with high doses of LT resulted in a sustained decline in full-length mitogen-activated protein kinase kinase 2, a known target of lethal factor, and a marked reduction in diphosphorylated extracellular response kinases 1,2 for 24 h. However, despite the sustained loss of full-length mitogen-activated protein kinase kinase 2, by 48 h, TIR macrophages regained diphosphorylated extracellular response kinases 1,2, suggesting an adaptation led to recovery of this signaling pathway. TIR macrophages were also able to maintain normal levels of ubiquitinylated proteins, whereas sensitive cells show a rapid reduction in ubiquitin-modified proteins before cell death, indicating a possible alteration in proteasome activity contributed to resistance. These results provide a paradigm for toxin-cell interactions and suggest macrophages are capable of adapting to and tolerating toxic doses of LT.

| S-EPMC218774 | biostudies-literature

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.

2011-09-07 | GSE28554 | GEO

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