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

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

PROVIDER: PRJNA765371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16013100.fastq.gz	Fastqsanger.gz
	SRR16013101.fastq.gz	Fastqsanger.gz
	SRR16013102.fastq.gz	Fastqsanger.gz
	SRR16013103.fastq.gz	Fastqsanger.gz
	SRR16013104.fastq.gz	Fastqsanger.gz

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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

Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2<sup>+</sup> DRG sensory neurons.

Project description:Bacterial products can act on neurons to alter signaling and function. In the present study, we found that dorsal root ganglion (DRG) sensory neurons are enriched for ANTXR2, the high-affinity receptor for anthrax toxins. Anthrax toxins are composed of protective antigen (PA), which binds to ANTXR2, and the protein cargoes edema factor (EF) and lethal factor (LF). Intrathecal administration of edema toxin (ET (PA + EF)) targeted DRG neurons and induced analgesia in mice. ET inhibited mechanical and thermal sensation, and pain caused by formalin, carrageenan or nerve injury. Analgesia depended on ANTXR2 expressed by Nav1.8+ or Advillin+ neurons. ET modulated protein kinase A signaling in mouse sensory and human induced pluripotent stem cell-derived sensory neurons, and attenuated spinal cord neurotransmission. We further engineered anthrax toxins to introduce exogenous protein cargoes, including botulinum toxin, into DRG neurons to silence pain. Our study highlights interactions between a bacterial toxin and nociceptors, which may lead to the development of new pain therapeutics.

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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

DRG from CCI and Seltzer models of neuropathic pain and sham operated animals

Project description:L5 DRG samples from CCI, Seltzer and sham models collected at 14, 21 and 50 days after surgery from ipsilateral hind limb. Note that all replicates are techincal, i.e., there were no biological replicates in this study as samples were pooled for each group Keywords: ordered

2005-05-21 | GSE2636 | GEO

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.

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scRNA-sequencing reveals subtype-specific transcriptomic perturbations in DRG neurons of PirtEGFPf mice in neuropathic pain condition

Project description:Functionally distinct subtypes/clusters of dorsal root ganglion (DRG) neurons may play different roles in nerve regeneration and pain. However, details about their transcriptomic changes under neuropathic pain conditions remain unclear. Chronic constriction injury (CCI) of the sciatic nerve represents a well-established model of neuropathic pain, and we conducted single-cell RNA-sequencing (scRNA-seq) to characterize subtype-specific perturbations of transcriptomes in lumbar DRG neurons on day 7 post-CCI. By using PirtEGFPf mice that selectively express an enhanced green fluorescent protein in DRG neurons, we established a highly efficient purification process to enrich neurons for scRNA-seq. We observed the emergence of four prominent CCI-induced clusters and a loss of marker genes in injured neurons. Importantly, a portion of injured neurons from several clusters were spared from injury-induced identity loss, suggesting subtype-specific transcriptomic changes in injured neurons. Moreover, uninjured neurons, which are necessary for mediating the evoked pain, also demonstrated cell-type-specific transcriptomic perturbations in these clusters, but not in others. Notably, male and female mice showed differential transcriptomic changes in multiple neuronal clusters after CCI, suggesting transcriptomic sexual dimorphism in DRG neurons after nerve injury. Using Fgf3 as a proof-of-principle, RNAscope study provided further evidence of increased Fgf3 in injured neurons after CCI, supporting scRNA-seq analysis, and calcium imaging study unraveled a functional role of Fgf3 in neuronal excitability. These findings may contribute to the identification of new target genes and the development of DRG neuron cell-type-specific therapies for optimizing neuropathic pain treatment and nerve regeneration.

2022-10-24 | GSE216039 | GEO

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

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

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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