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Transcriptome changes in IL-10 treated peritoneal macrophages

ABSTRACT: To try to identify the mechanism of STAT3s indirect action we have used a genomic approach to map the binding sites of STAT3 within the genome and also used RNA-seq technology to map the changes in RNA expression and transcript isoform abundance in response to IL-10.

ORGANISM(S): Mus musculus

PROVIDER: GSE31530 | GEO | 2012/02/13

SECONDARY ACCESSION(S): PRJNA154983

REPOSITORIES: GEO

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Transcriptome changes in IL-10 treated peritoneal macrophages

Project description:To try to identify the mechanism of STAT3s indirect action we have used a genomic approach to map the binding sites of STAT3 within the genome and also used RNA-seq technology to map the changes in RNA expression and transcript isoform abundance in response to IL-10. Examination of transcriptome changes in peritoneal macrophages when treated with IL-10 for 4 hours. RNA was extracted and sequenced.

2012-02-13 | E-GEOD-31530 | biostudies-arrayexpress

Genome-wide binding of STAT3 in peritoneal macrophages

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Project description:To try to identify the mechanism of STAT3âs indirect action we have used a genomic approach to map the binding sites of STAT3 within the genome and also used RNA-seq technology to map the changes in RNA expression and transcript isoforms in response to IL-10. Examination of STAT3 binding by ChIP-seq in Unstimulated and IL-10 treated peritoneal exudate macrophages purified from mice. We sequenced anti-STAT3 ChIP-seq as well as corresponding control (Input) libraries

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RNA-seq analysis of IL-10 treatment of wildtype and Ptpn1-/- knockout peritoneal macrophages

Project description:We report here the deep sequencing of the mRNA from peritoneal exudate cells (macrophages) purified from wildtype or Ptpn1 (PTP1B) knockout mice, either treated or untreated with IL-10. In periotenal macrophages IL-10 activates the transcription factor STAT3 to execute and anti-inflammatory gene expression programme. The tyrosine phosphatase PTPN1 targets STAT3 for dephosphorylation and leads to the deactivation of STAT3. In this study we examined the role of PTP1B in controlling the normal homeostatic level phosphorylation of STAT3 by comparing the IL-10/STAT3-mediated anti-inflammatory gene expression programme. We find that loss of PTP1B leads to an up-regulation of the activity of STAT3, both at the level of phosphorylation and also in enhanced expression of anti-inflammatory gene products. RNA-seq of wildtype and Ptpn1 (PTP1B) knockout mouse peritoneal macrophages, treated or untreated with IL-10

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RNA-seq analysis of IL-10 treatment of wildtype and Ptpn1-/- knockout peritoneal macrophages

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Genome-wide analysis of STAT3-binding and gene expression changes in peritoneal macrophages upon interleukin-10 stimulation

Project description:This SuperSeries is composed of the following subset Series: GSE31529: Genome-wide binding of STAT3 in peritoneal macrophages GSE31530: Transcriptome changes in IL-10 treated peritoneal macrophages Refer to individual Series

2012-02-13 | E-GEOD-31531 | biostudies-arrayexpress

Dynamic genome-wide transcriptional response of human monocyte-derived dendritic cells to IL-6 and Il-10

Project description:Single cell timecourse experiments demonstrated that though IL-6 and IL-10 activate STAT3, they generate different temporal patterns of activation, with IL-6 generating a transient activation of STAT3, and IL-10 generating a sustained STAT3 response. We hypothesized that these different STAT3 activation dynamics would dictate the differing cellular responses to the two cytokines. Human monocyte-derived denditic cells from four different donors were treated with IL-6 or IL-10 for either 0min, 45min, 2hr, 4hr, 8hr, or 12hr. Total RNA was isolated from each sample and used for gene expression analysis.

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Project description:Septic peritonitis remains a major cause of death. Neutrophils and inflammatory monocytes are principal components of the innate immune system and are essential for defense against a range of microbial pathogens. Their role and interaction in polymicrobial sepsis have not been defined clearly. Using a murine model of CLP to induce moderate sepsis, we found that neutrophil depletion did not alter survival, whereas depletion of neutrophils and inflammatory monocytes markedly reduced survival. After neutrophil depletion, inflammatory monocytes had greater phagocytic capacity and oxidative burst, and increased expression of costimulatory molecules, TNF, and iNOS. Notably, peritoneal neutrophils produced IL-10 following CLP. Adoptive i.p. transfer of WT but not IL-10(-/-) neutrophils into septic mice reduced monocyte expression of TNF. In vitro experiments confirmed that monocyte suppression was mediated by neutrophil-derived IL-10. Thus, during septic peritonitis, neutrophils suppress peritoneal inflammatory monocytes through IL-10 and are dispensable for survival.

| S-EPMC3040467 | biostudies-literature

Dynamic genome-wide transcriptional response of human monocyte-derived dendritic cells to IL-6 and Il-10

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