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PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

ABSTRACT: PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

PROVIDER: PRJNA481067 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7521790.fastq.gz	Fastqsanger.gz
	SRR7521800.fastq.gz	Fastqsanger.gz
	SRR7521791.fastq.gz	Fastqsanger.gz
	SRR7521801.fastq.gz	Fastqsanger.gz
	SRR7521792.fastq.gz	Fastqsanger.gz

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Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

Project description:Systemic lupus erythematosus (SLE) is characterized by upregulation of Type Ι Interferon (IFN) and widespread inflammation. However, blocking the IFN pathway benefits a fraction of patients, pointing to additional pathogenic players. Here we describe monocytes (Mo) undergoing erythrophagocytosis and co-expressing IFN-inducible genes (ISGs) and interleukin-1b (IL-1b) in patients with active disease. This phenotype is recapitulated in vitro upon internalization of red blood cells carrying mitochondria (Mito+ RBCs), a feature of SLE. While ISG expression requires the interaction between Mito+ RBC-derived mitochondrial DNA (mtDNA) and cGAS, the production of IL-1b entails Mito+ RBC-derived mitochondrial RNA (mtRNA) triggering RIG-I-like receptor (RLR) activation. This leads to the cytosolic release of Mo-derived mtDNA and activation of the NLRP3 inflammasome. Importantly, the Type I IFN-inducible protein myxovirus resistant protein 1 (MxA) enables IL-1b release by routing this cytokine into a trans-Golgi network (TGN)-mediated unconventional secretory pathway. As Type I IFN and IL-1b are thought to counter-regulate each other, our study highlights an unprecedented synergy between these two cytokine pathways in SLE.

2024-10-07 | GSE211361 | GEO

PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

Project description:TG elicited Peritoneal macrophages from WT and PPARgamma KO mice were treated with control or lipid inflammatory stress in triplicate

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Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

Project description:Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

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Long non-coding RNAs are central regulators of the IL-1b-induced inflammatory response in human lung fibroblasts

Project description:There is accumulating evidence to indicate that long non-coding RNAs (lncRNAs) are important regulators of the inflammatory response. In this report, we have employed next generation sequencing to identify 14 lncRNAs that are differentially expressed in human lung fibroblasts following the induction of inflammation using interleukin-1b (IL-1b). Knockdown of the two most highly expressed lncRNAs, IL7AS and MIR3142HG, showed that IL7AS negatively regulated IL-6 release whilst MIR3142HG was required for IL-8 and CCL2 release. Parallel studies in fibroblasts derived from patients with idiopathic pulmonary fibrosis showed similar increases in IL7AS levels, that also negatively regulate IL-6 release. In contrast, IL-1b-induced MIR3142HG expression was reduced by 8-fold in IPF fibroblasts, with the consequence being that MIR3142 knockdown showed no effect upon IL-8 and CCL2 release. In summary, we have catalogued those lncRNAs that are differential expression following IL-1b-activation of human lung fibroblasts and shown that these regulate the inflammatory response.

2018-10-16 | GSE121241 | GEO

Placental PPARg-Regulated Genes

2012-07-10 | GSE39233 | GEO

Cell line stimulated with recombinant cytokines interleukin-1b and interferon gamma.

Project description:Interleukin 1b and interferon g are two cytokines that are central to the inflammatory response. They both have a broad range of activity, each directing the immune response to be towards either the innate response (IL-1b and IFN-g) or the cellular response (IFN-g), however invivo there is a lot of subtle interactions. Microarray analysis has been used to characterize the transcriptional response to recombinant rainbow trout IL-1b and IFN-g in a rainbow trout macrophage cell line RTS-11. The use of the cell line removes the host response and the interference of other cellular factors that occur when performing whole fish experiments, or even primary cultures. RNA was extracted from stimulated or control cells following 6h incubation, this was used to hybridize to a 16K v1 salmonid cDNA array constructed by GRASP consortium. Keywords: Dual label cDNA microarray

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Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix. 3 PPARg +/- LysCre and 3 PPARg fl/- LysCre mice were used to isolate bone marrow and from each macrophages were differentiated with or without IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 24 samples with 3 biological replicates as below.

2010-11-18 | E-GEOD-25123 | biostudies-arrayexpress

PPARG interactions with UBR5 and MRE11-RAD50-NBS1 are required for DNA damage response and repair.

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