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Interleukin 1b triggers catabolism via a central nervous system-mediated pathway in mice and rat

ABSTRACT: Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays.

ORGANISM(S): Mus musculus

PROVIDER: GSE26766 | GEO | 2011/11/03

SECONDARY ACCESSION(S): PRJNA136303

REPOSITORIES: GEO

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Interleukin 1b triggers catabolism via a central nervous system-mediated pathway in mice and rat

Project description:Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays. 28 samples were analyzed. The following comparisons were made: 6 groups were defined on the basis of treatment and time. Differences between groups were assesed by one way-ANOVA. P values were corrected for multiple comparisons using the Benjamini Hochberg correction at a false discovery rate of 1%. Probes were considered that showed a 1.75 fold or greater up or down regulation at any of the three timepoints.

2011-11-03 | E-GEOD-26766 | biostudies-arrayexpress

Transcription profiling of mouse hippocampus treated with intracerebroventricular administration of LPS in a vehicle controlled experiment

Project description:Effect of icv (intracerebroventricular) administration of LPS in mice in a vehicle controlled experiment. After administrating LPS icv, the hippocampus is dissected out and inflammatory gene inductions are chip analyzed

2005-10-01 | E-MEXP-472 | biostudies-arrayexpress

Transcription profiling of effect of icv administration of LPS (4 + 16 hr) on mouse hippocampal and microgial samples

Project description:Effect of icv (intracerebroventricular) adminstration of LPS (vehicle controled) evaluated both, 4 and 16 hours after the injection.

2006-01-01 | E-MEXP-420 | biostudies-arrayexpress

Pdx1 overexpression sensitizes to IL-1b-induced apoptosis

Project description:Cytokines have been shown to play a key role in the destruction of beta cells. In the rat insulinoma cell line (INS-1ab) overexpressing pancreatic duodenum homeobox 1 (Pdx1) increases sensitivity to Interleukin 1b (IL-1b). To elucidate mechanisms of action underlying Pdx1 driven potentiation of beta-cell sensitivity to IL-1β, we performed a microarray analysis of INS-1ab cells with and without Pdx1 overexpression exposed to IL-1β between 2h and 24h. INS-1ab cells were cultured with or without 500 ng/ml doxycycline (+/- DOX). After 24 h, 40 ng/ml IL-1b was either added or not (+/- IL-1b). Cells were harvested either 2h, 4h, 6h, 12h or 24h after addition of IL-1b. Four biological replicates for each of the eight groups.

2012-09-20 | E-GEOD-40642 | biostudies-arrayexpress

Transcriptome of human ILC2s; primary vs IL-1b-primed

Project description:ILC2s regulate type2 immune responses and protect against helminth infection. We found that ILC2s can be expanded in the presence of a combination of cytokines IL-2 and IL-1b. To better understand the functional and phenotypic consequence of IL-1β activation of ILC2s, we utilized whole transcriptome sequencing (RNA-seq) of freshly isolated ILC2s and IL-1β-primed ILC2s. Differential expression analysis revealed a substantial number of genes underwent significant change between the two conditions (total 4,744 gene, FDR<0.01, Fold change >2), among which 3,871 genes were upregulated in IL-1β –primed ILC2s.

2016-04-25 | GSE72460 | GEO

IL-1B signaling in dendritic cells induces antiviral interferon responses

Project description:Activation of interferon-stimulated gene (ISG) responses is critical for control of viral infection. We recently identified that stimulation of the NLRP3 inflammasome and mobilization of the inflammatory cytokine IL-1β act as critical host restrictive pathways against West Nile virus (WNV) in a mechanism dependent on the regulation of ISGs. In order to define the mechanism by which IL-1β regulates these antiviral immune programs, we utilized global transcriptome analysis in myeloid cells, known targets of WNV replication to define gene signatures required for IL-1β driven antiviral responses. Surprisingly, we found IL-1β dependent activation of interferon-beta (IFN-β) and ISGs at late times following IL-1β treatment. Expression of these antiviral innate immune genes was found to be dependent on activation of IRF3 and appears to reflect a general shift in IL-1β signaling from an inflammatory response early following treatment to an anti-inflammatory type-I IFN mediated response at later times post-treatment. These data demonstrate that inflammatory and antiviral signals integrate to control viral infection. Strategies to co-opt these cytokine activated antiviral signatures can act as novel targeted therapeutic strategies tailored specifically to individual pathogens.

2018-01-12 | GSE109069 | GEO

Expression Data from hypothalamus of IL-6 deficient mice and their wild-type littermates following intraperitoneal LPS challenge

Project description:IL-6 has been described to be a critical cytokine in mediating the febrile response because neither IL-6 knockout mice injected with peripheral lipopolysaccharide (LPS) or IL-1β, nor animals treated with IL-6 antiserum develop fever. However, the fever response is developed in IL-6 KO mice following intracerebroventricular administration of Prostaglandin E2 which is the principal mediator of the febrile response.

2012-10-29 | GSE34673 | GEO

Ribosome profiling of chondrocytic cell line SW1353 following exposure to IL-1B

Project description:Osteoarthritis is a chronic disease characterised by the loss of articular cartilage in synovial joints through a process of extracellular matrix destruction that is strongly associated with inflammatory stimuli. Chondrocytes undergo changes to their protein translation capacity during osteoarthritis, but a study of how disease-relevant signals effect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study we describe how the inflammatory cytokine interleukin 1-beta (IL-1β) rapidly affects protein translation in the chondrocytic cell line SW1353. Using ribosome profiling we demonstrate that IL-1β induced altered translation of inflammatory-associated transcripts such as NFKB1, TNFAIP2, MMP13, CCL2 and CCL7, as well as a number of ribosome-associated transcripts, through differential translation and the use of multiple open reading frames. Proteomic analysis of the cellular layer and the conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. These translationally regulated secreted proteins included a number of chemokines and cytokines, underlining the rapid, translationally-mediated inflammatory cascade that is initiated by IL-1 β.

2019-07-12 | E-MTAB-7466 | biostudies-arrayexpress

Pdx1 overexpression sensitizes to IL-1b-induced apoptosis

2012-09-20 | GSE40642 | GEO

Transcriptome response to 4h IL-1b stimulation of primary chondrocytes

Project description:Using RNA sequencing (Illumina Hi-Seq 2000 sequencer) we report the transcriptome profile of primary human chondrocytes isolated from patients with hip osteoarthritis (OA), and the transcriptome response of these cells to 4h stimulation with IL-1β (1ng/ml). In total, 983 long non-coding RNAs (lncRNAs) were identified, which included 642 intergenic lncRNAs (lincRNAs), 124 antisense and pseudogenes. Less than 4% of the identified lncRNAs overlapped with putative eRNAs regions, and visual inspection showed that they were uni-directional and multi-exonic. Upon IL-1β stimulation 499 protein-coding genes were differentially expressed, and 158 lncRNAs were differentially expressed, including 92 lincRNAs, 13 antisense and 18 psudogenes. This study demonstrates that IL-1β induces a rapid and widespread change in the transcriptome of the primary human OA chondrocyte.

2015-10-21 | GSE74220 | GEO

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