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

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

PROVIDER: PRJNA603770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10985237_1.fastq.gz	Fastqsanger.gz
	SRR10985237_2.fastq.gz	Fastqsanger.gz
	SRR10985238_1.fastq.gz	Fastqsanger.gz
	SRR10985238_2.fastq.gz	Fastqsanger.gz
	SRR10985239_1.fastq.gz	Fastqsanger.gz

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

2020-02-17 | GSE144481 | GEO

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

2020-02-17 | GSE144482 | GEO

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

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

| PRJNA603763 | ENA

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

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

| PRJNA603768 | ENA

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

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 κB (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 proinflammatory mediators, including tumor necrosis factor-α (TNF-α), by bone marrow 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. Rather, 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, 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 hyperinflammatory state. We hypothesize that inflammatory cytokine production by neutrophils may contribute to leukemia associated with inherited RUNX1 mutations.

| S-EPMC7094023 | biostudies-literature

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-02-17 | GSE144483 | GEO

Transcriptome comparison of PMN-MDSCs and and normal neutrophils

Project description:Polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), also named pathologically activated neutrophil, is a critical component of tumor microenvironment (TME), playing crucial roles in tumor progression and therapy resistance. Here, we compared the transcriptome of PMN-MDSCs from B16 tumor bearing mice and the neutrophils from tumor free mice.

2023-06-26 | GSE199601 | GEO

Whole genome expression profile of human decidual PMN-MDSC and autologous neutrophils in normal pregnancy

Project description:It is suggested that decidual polymorphonuclear myeloid-derived suppressor cell (PMN-MDSCs) are a group of activated suppressive neutrophils. Decidual microenvironment can facilitate circulating neutrophils with phenotypes and functions of PMN-MDSCs. The mechanism of PMN-MDSCs differentiation induced by decidual microenvironment has not been fully understood. Here we performed whole genome expression profile of 3 decidual PMN-MDSCs and autologous neutrophils from normal early pregnancy. Total RNA were extracted. The arrays were scanned by the Agilent Scanner G2505C. There were differences of gene expression pattern between decidual PMN-MDSCs and autologous neutrophils in early normal pregnancy.

2022-05-13 | GSE192850 | GEO

lncRNA-CR11538 functions as a decoy of Dif/Dorsal to negatively regulate Drosophila Toll immune responses

Project description:The maintenance of innate immune homeostasis is critical for animal survival to combat pathogens. Although many positive or negative protein factors have been identified, little is known about the long non-coding RNA that regulates the Toll pathway. Herein, we have discovered a novel lncRNA-CR11538 highly activated during the Drosophila response to gram+ bacterial infection. The transient overexpression of CR11538 inhibited the expression of antimicrobial peptides (Drosomycin and Metchnikowin) in vivo to suppress Toll signaling pathway. Remarkably, core enrichment genes based on RNAseq, subcellular localization and RIP suggest that CR11538 can interact with the transcription factor Dif/Dorsal in nucleus. ChIP-qPCR and dual luciferase report experiments show that CR11538 can sequester Dif/Dorsal away from the promoter thus suppressing the transcription of antimicrobial peptides. In summary, we discovered a novel lncRNA-CR11538 that negatively regulate the Drosophila Toll pathway. It broadens our understanding of the regulatory mechanism of Toll pathway involving lncRNA and provides insights for the research on innate immune system of insects and mammals.

2021-08-13 | GSE181870 | GEO

Transcriptome comparison of PMN-MDSCs and and normal neutrophils

Project description:Transcriptome comparison of PMN-MDSCs and and normal neutrophils

| PRJNA820788 | ENA