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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE86169 | GEO | 2017/02/09

SECONDARY ACCESSION(S): PRJNA340446

REPOSITORIES: GEO

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

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.

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

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Difference of gene expression between LPS-stimulated monocytes cultured in the presence NRBCs and those cultured in the absence of NRBCs

Project description:We found that human cord blood nucleated red blood cells (NRBCs) have a regulatory function in the innate immune reaction. NRBCs suppressed the production of inflammatory cytokines including TNF-a and IL-1b from monocytes in response to lipopolysaccharide (LPS). NRBCs exerted the regulatory function even without cell-to-cell contact with monocytes. On the other hand, IL-10 production from monocytes by the stimulation of LPS in the presence of NRBCs was higher than that of LPS-stimulated monocytes cultured in the absence of NRBCs. Addition of an anti-IL-10 receptor blocking antibody restored the inflammatory cytokine production from monocytes, suggesting that the functional change of monocytes caused by the interaction of NRBCs was characterized and mediated by the increased IL-10 production. Whole-genome microarray analysis revealed that monocytes expressed increased amounts of IL-10 superfamily genes after the interaction with NRBCs. IL-19, one of the IL-10 superfamily, enhanced IL-10 production from monocytes, which suggested cooperative role of IL-10 superfamily in the suppression of inflammatory cytokine production from monocytes. Arginase which was reported to play an important role in the suppressive function of NRBCs on monocytes in mice was found to play no significant role in human monocytes. NRBCs seem to have a regulatory role to suppress vigorous innate immune reaction which can be harmful to the fetuses via some unknown soluble factor which enhances the production of IL-10 and IL-10 family cytokines in monocytes. Human LPS-stimulated monocytes were collected after culture in a condition without and with NRBCs in transwell culture system. Only one experiment was performed.

2015-12-31 | E-GEOD-70146 | biostudies-arrayexpress

Difference of gene expression between LPS-stimulated monocytes cultured in the presence NRBCs and those cultured in the absence of NRBCs

2015-12-31 | GSE70146 | GEO

A 17 kDa fragment of lactoferrin associates with the termination of inflammation and peptides within promote resolution

Project description:During the resolution of inflammation macrophages engulf apoptotic polymorphonuclear cells (PMN) and can accumulate large numbers of their corpses. Here we report that resolution-phase-macrophages acquire the neutrophil-derived glycoprotein lactoferrin (Lf) in vivo and ex vivo and process it to short fragments. During the onset and resolving phases of inflammation in murine peritonitis and bovine mastitis Lf fragments of 15 and 17 kDa occurred in various body fluids, and the murine fragmentation and release were mediated by macrophages. The 17 kDa fragment contained two bioactive tripeptides, FKD and FKE that promoted human macrophage reprogramming to a pro-resolving phenotype. At low concentrations (1-10 M) this was reflected by inhibition of LPS-induced TNFand IL-6 secretion and increased IL-10 levels. Both peptides inhibited ERK and cJun activation following macrophage exposure to LPS. In addition, FKD, and to a lesser extent FKE, promoted neutrophil-mediated resolution at high concentrations (30-100 M) by enhancing the formation of cytokine-scavenging aggregated NETs at low cellular density. Thus, PMN lactoferrin is acquired, processed and

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Genome-wide RNA sequencing analysis in Il10-/- bone marrow-derived macrophages stimulated by lipopolysaccharide

Project description:We report the genome-wide RNA sequencing analysis in Il10-/- bone marrow-derived macrophages (BMDMs) stimulated by lipopolysaccharide (LPS) where IL-10 effect in macrophage inflammatory response was examined in IL-10-deficient BMDMs upon LPS stimulation with addition of exogenous IL-10.

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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

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Gene expression profiles of mice BMDCs treated with Nitidine Chloride or vehicle following LPS stimulation

Project description:Nitidine Chloride(NC) were found to enhance IL-10 production in LPS-stimulated Bone-marrow dendritic cells(BMDCs ) ,while at the same time inhibit pro-inflammatory cytokines production, such as TNF- α and IL-6. BMDCs were treated with NC or vehicle following LPS stimulation to find out the influence of NC on BMDCs that regulate cytokines expression. This study indicated that NC regulate numerous gene expression, thus influence IL-10 and pro-inflammatory cytokines production in LPS-treated BMDCs.

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Control of LPS-response by DUSP1

Project description:Activation of the Mitogen activated protein kinase (MAPK) cascade following Toll-like receptor (TLR) stimulation enables innate immune cells to rapidly activate cytokine gene expression. A balanced response to signals of infectious danger requires that cellular activation is transient. Here, we identify the MAPK phosphatase Dual specificity phosphatase-1 (DUSP1) as an essential endogenous regulator of the inflammatory response to LPS. DUSP1-deficient (DUSP1-/-) bone marrow derived macrophages showed selectively prolonged activation of p38 MAPK and increased cytokine production. Intraperitoneal challenge of DUSP1-/- mice with LPS caused increased lethality and overshooting production of IL-6 and TNF?. Transcriptional profiling revealed that DUSP1 controls a significant fraction of LPS-induced genes, that includes IL-6 and IL-10 as well as the chemokines CCL3, CCL4 and CXCL2. In contrast, the expression of the important mediators of endotoxin lethality, IFN? and IL-12, was not significantly altered by the absence of DUSP1. These data together demonstrate a specific regulatory role of DUSP1 in controlling a subset of LPS-induced genes that determines the outcome of endotoxin shock. Keywords: in vivo analysis of splenic mRNA expression

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