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Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation

ABSTRACT: Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation

PROVIDER: PRJNA340393 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4090200.fastq.gz	Fastqsanger.gz
	SRR4090330.fastq.gz	Fastqsanger.gz
	SRR4090340.fastq.gz	Fastqsanger.gz
	SRR4090201.fastq.gz	Fastqsanger.gz
	SRR4090331.fastq.gz	Fastqsanger.gz

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Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation [stat3_ChIP]

Project description:IL-10 limits the magnitude of inflammatory gene expression following microbial stimuli and is essential to prevent inflammatory disease, however, the molecular basis for IL-10 mediated inhibition remains elusive. Using a genome-wide approach we demonstrate that inhibition of transcription is the primary mechanism for IL-10-mediated suppression in LPS-stimulated macrophages, and that inhibited genes can be divided into two clusters. Genes in the first cluster are inhibited only if IL-10 is included early in the course of LPS stimulation and is strongly enriched for interferon-inducible genes. Genes in the second cluster can be rapidly suppressed by IL-10 even after transcription is initiated, and this is associated with suppression of LPS-induced enhancer activation. Interestingly, the ability of IL-10 to rapidly suppress active transcription exhibits a delay following LPS stimulation. Thus, a key pathway for IL-10 mediated suppression involves rapid inhibition of enhancer function during the secondary phase of the response to LPS.

2017-02-09 | GSE86169 | GEO

Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation [h3k27 ChIP]

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Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation [RNA-Seq]

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IL-10 or IL-6 stimulation of IL-6-/- and IL-10-/- murine bone marrow derived macrophages in the presence of LPS

Project description:IL-10 or IL-6 stimulation of control 129xC57BL/6 murine bone marrow derived macrophages in the presence of LPS. We used microarrays to detail the global programme of gene expression changes in response to IL-6 or IL-10 stimulation in the presence of lipopolysaccharide. BMDMs were isolated from control, IL-6-/-, and IL-10-/- mice on a 129XBL/6 mixed background mice and differentiated in the presence of CSF-1 for 6-7 days. Cells were scraped and plated in 6 well plates at 2x10e6/well. Cells were washed with complete DMEM and rested for 1-2 hr before stimulation with combinations of IL-10 (10 ng/ml), IL-6 (2 ng/ml) or LPS (100 ng/ml) for 45 min or 180 mins. Complete biological replicates were performed. Keywords: time course

2006-08-25 | GSE5589 | GEO

Transcription profiling of mouse bone marrow macrophages from IL-6-/- and IL-10-/- mutants treated with IL-10 or IL-6 stimulation in the presence of LPS

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Transcription profiling of mouse IL-10 -/- macrophages treated with LPS/LPS plus IL10 reveals a transcriptional repressor and co-repressor induced by the STAT3-regulated anti-inflammatory signaling pathway.

Project description:IL-10 regulates anti-inflammatory signaling via the activation of STAT3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on pro-inflammatory mediator production. Here we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3 and a helicase family co-repressor, SBNO2 (Strawberry notch homolog 2) in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3, and co-stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway induced by IL-10 but not STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 specifically repressed NF-kB-mediated transcription and can physically interact. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10. We compared expression profiles of macrophages isolated from IL-10 -/- mice. Macrophages were treated with either LPS or LPS plus IL-10. Treatment times were 10, 20 and 30 minutes. Experiment Overall Design: Mouse IL-10 -/- macrophages were isolated and purified and set up in culture medium containing LPS or LPS plus IL-10. A total of 18 samples were analyzed. This set contains three replicates of each treatment condition where treatment (LPS versus LPS plus IL-10) and time (10min, 20min and 30min) were varied.

2008-06-16 | E-GEOD-9509 | biostudies-arrayexpress

The effects of IL-10 on the gene expression of LPS-activated activated dendritic cells

Project description:Gene expression profiels in the human monocyte-derived dendritic cells (DCs) from 4 different donors (A, B, C, and D) were studied. Cells were left untreated (Group 4), activated with LPS alone (Group 1) or activated in the presence cmv IL-10 (Group 2) or human IL-10 (Group 3) for 12 hours before subjected to RNA extraction. Keywords: IL-10, LPS, dendritic cells

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Inhibition of inflammatory gene transcription by IL-10 is associated with rapid suppression of LPS-induced enhancer activation

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

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Transcriptional effects of IL-10 neutralization on LPS-activated M-CSF-derived macrophages

Project description:Analysis of the role of IL-10 on the transcriptional signature of LPS-activated human M-CSF-dependent monocyte-derived macrophages. Methods: Human Peripheral Blood Mononuclear Cells (PBMC) were isolated from buffy coats from donors over a Lymphoprep gradient according to standard procedures. Monocytes were purified from PBMC by magnetic cell sorting using anti-CD14 microbeads (>95% CD14+ cells). Monocytes from three independent donors (0.5 x 106 cells/ml, >95% CD14+ cells) were cultured in RPMI 1640 supplemented with 10% fetal bovine serum (FBS) at 37°C in a humidified atmosphere with 5% CO2 and 21% O2 for 7 days in the presence of 1000 U/ml M-CSF, with cytokine addition every two days. Then, monocyte-derived macrophages were treated with an anti-IL-10 blocking antibody (anti-IL10) or an isotype-matched antibody (IgG2b) at 2.5 micrograms/ml for 1 hour, and exposed to LPS (10 ng/ml). After 4 hours of LPS treatment, cells were lysed and RNA isolated for transcriptional analysis.

2022-06-08 | GSE181250 | GEO

microRNA responses of LPS and IL-10 stimulated primary human monocyte-derived macrophages over a short time-course

Project description:Lipopolysaccharide stimulated primary human monocyte-derived macrophages at 2, 4 and 8hrs, IL-10 at 4hrs, IL-10+LPS at 4hrs

2019-01-25 | GSE125572 | GEO