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Transcriptional profiling of mouse neutrophils treated ex vivo with a Toll-like receptor 5 agonist

ABSTRACT: Transcriptional profiling of mouse neutrophils treated ex vivo with a Toll-like receptor 5 agonist

PROVIDER: PRJNA745157 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15084871.fastq.gz	Fastqsanger.gz
	SRR15084872.fastq.gz	Fastqsanger.gz
	SRR15084873.fastq.gz	Fastqsanger.gz
	SRR15084874.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of mouse neutrophils treated ex vivo with a Toll-like receptor 5 agonist

Project description:Acute radiation syndrome (ARS) is a major cause of lethality following radiation disasters. A TLR5 agonist, entolimod, is among the most powerful experimental radiation countermeasures and shows efficacy in rodents and non-human primates as a prophylactic (radioprotection) and treatment (radiomitigation) modality. While the prophylactic activity of entolimod has been connected to suppression of radiation-induced apoptosis, the mechanism by which entolimod functions as a radiomitigator remains poorly understood. Here, we demonstrate that, in contrast to radioprotection, neutrophils are essential for the radiomitigative activity of entolimod. We found that neutrophils express functional TLR5 and stimulation by entolimod is a key component to the mechanism of radiomitigation. Given that the underlying effects of TLR5 agonists have been associated with NF-kB-dependent transcriptional events, we hypothesized that changes in the transcriptional profile of neutrophils post-entolimod treatment mitigates radiation damage. However, RNA sequencing data analysis showed that ex vivo stimulation of neutrophils with entolimod for 30 minutes caused changes in transcriptional profiles that were substantially weaker – both in the number of responsive genes and scale of changes – as compared with that of liver cells following in vivo entolimod treatment. These observations suggest that mitigation of radiation damage by entolimod-stimulated neutrophils involves a transcriptional-independent mechanism.

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The ex vivo productionofmature neutrophils depends on the sourceofCD34+ human hematopoietic progenitors

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Toll-like receptor agonist CBLB502 protects against radiation-induced intestine injury in mice

Project description:Toll-like receptor agonist CBLB502 protects against radiation-induced intestine injury in mice

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Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling: HP scRNA-seq

Project description:RUNX1 is frequently mutated in myeloid and lymphoid malignancies. It has been shown to negatively regulate Toll-like receptor 4 (TLR4) signaling through nuclear factor kappa-B (NF-κB) in lung epithelial cells. Here we show that RUNX1 regulates TLR1/2 and TLR4 signaling and inflammatory cytokine production by neutrophils. Hematopoietic-specific RUNX1 loss increased the production of pro-inflammatory mediators, including tumor necrosis factor α (TNF-α), by bone marrow (BM) neutrophils in response to TLR1/2 and TLR4 agonists. Hematopoietic RUNX1 loss also resulted in profound damage to the lung parenchyma following inhalation of the TLR4 ligand lipopolysaccharide (LPS). However, neutrophils with neutrophil-specific RUNX1 loss lacked the inflammatory phenotype caused by pan-hematopoietic RUNX1 loss, indicating that dysregulated TLR4 signaling is not due to loss of RUNX1 in neutrophils per se, and single cell RNA sequencing indicates the dysregulation originates in a neutrophil precursor. Enhanced inflammatory cytokine production by neutrophils following pan-hematopoietic RUNX1 loss correlated with increased degradation of the inhibitor of NF-κB signaling (IκBα), and RUNX1-deficient neutrophils displayed broad transcriptional upregulation of many of the core components of the TLR4 signaling pathway. Hence early, pan-hematopoietic RUNX1 loss de-represses an innate immune signaling transcriptional program that is maintained in terminally differentiated neutrophils, resulting in their hyper-inflammatory state. We hypothesize that inflammatory cytokine production by neutrophils may contribute to leukemia associated with inherited RUNX1 mutations.

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Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling: PMN bulk RNA-seq

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The ex vivo productionofmature neutrophils depends on the sourceofCD34+ human hematopoietic progenitors

Project description:The ex vivo productionofmature neutrophils depends on the sourceofCD34+ human hematopoietic progenitors

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Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling

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