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Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

ABSTRACT: To validate the modulation of inflammatory genes by ectopic IL-33, we performed Gene expression analysis using the nCounter Mouse v2 Inflammation Panel. This result validated a significant increase in a number of anti-inflammatory cytokines in the IL-33+ xenografts that were absent in the DNLS xenografts

ORGANISM(S): Mus musculus

PROVIDER: GSE153488 | GEO | 2020/08/21

REPOSITORIES: GEO

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Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Determination of the molecular mechanism of IL33 on glioma cells Since IL-33 is known to associate with chromatin and regulate transcriptional activity and that nuclear expression of IL-33 increases glioma progression, we determined Nuclear IL-33 regulates the expression and secretion of inflammatory cytokines in glioma cells. Using these parameters 340 genes were induced by the ectopic expression of IL-33 and an additional 377 genes were downregulated. Gene ontology terms over-represented in the genes induced by IL-33 include three major clusters that associate with cytokine activity and inflammation

2020-08-21 | GSE153486 | GEO

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

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A proteomic landscape of the spatiotemporal influence of Interleukin-33 (IL-33) in monocytes

Project description:Interleukin-33 (IL-33), a member of the IL-1 superfamily cytokines, is an endogenous danger signal and a nuclear-associated cytokine. It is one of the essential mediators of both innate and adaptive immune responses. Aberrant IL-33 signaling has been demonstrated to play a defensive role against various infectious and inflammatory diseases. Although the signaling responses mediated by IL-33 have been previously reported, the temporal signalingdynamicsare yet to be explored. Towards this end,we applied quantitative temporal phosphoproteomics analysis to elucidate pathways and proteins induced by IL-33 in THP1 monocytes. Employing TMT labeling-based quantitation and titanium dioxide (TiO2)-based phosphopeptide enrichment strategy followed by mass spectrometry analysis, we identified 14,515 phosphorylation sites mapping to 4,174 proteins across (0 min to 240 mins)time points.

2022-02-16 | PXD028673 | Pride

Dataset of spatiotemporal influences of interleukin IL-1 family cytokine: Interleukin-33 on cellular signal transduction pathways

Project description:Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. IL-33 signaling, from the early signaling events triggered by the ligand-activated receptor to result in activation of early and late signaling events, such as proteome changes. In this study, THP1 (monocyte) cell line model was stimulated with IL-33 (50 ng/ml) for varying duration (5, 10, 15, 30, 40, 60, 120 and 240 mins). We carried out in-depth proteomic analysis using high-resolution LC-MS/MS. Our analysis resulted in the identification of 64,030 peptides corresponding to 7947 protein groups. Differentially regulated proteins identified in this study could be targeted for developing an inflammatory immune response.

2022-02-17 | PXD024385 | Pride

Knockdown of interleukin-33 in human fibroblasts

Project description:Interleukin (IL)-33 is a cytokine that appears to mediate fibrosis by signaling via its receptor ST2 (IL-33R/IL1RL1). It is also, however, a protein that after synthesis is sorted to the cell nucleus, where it appears to affect chromatin folding. Here we describe a novel role for nuclear IL-33 in regulating the fibroblast phenotype in murine kidney fibrosis driven by unilateral ureteral obstruction. Transcriptional profiling of IL-33-deficient kidneys 24h after ligation revealed enhanced expression of fibrogenic genes and enrichment of gene sets involved in extracellular matrix formation and remodeling. These changes relied on intracellular effects of IL-33, because they were not reproduced by treatment with a neutralizing antibody to IL-33 that prevents IL-33R/ST2L receptor signaling nor were they observed in IL33R/ST2-deficient kidneys. To further explore the intracellular function of IL-33, we established transcription profiles of human fibroblasts, observing that knockdown of IL-33 skewed the transcription profile from an inflammatory towards a myofibroblast phenotype, reflected in higher levels of COL3A1, COL5A1 and transgelin protein, as well as lower expression levels of IL6, CXCL8, CLL7 and CCL8. In conclusion, our findings suggest that nuclear IL-33 in fibroblasts dampens the initial profibrotic response until persistent stimuli, as enforced by UUO, can override this protective mechanism.

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Transcriptional response of confluent human umbilical vein endothelial cells to stimulation with the related cytokines interleukin-1b or interleukin-33.

Project description:The similar response of endothelial cells to exogenous IL-33 or IL-1M-NM-2 prompted us to compare the genome-wide transcription profile of confluent human umbilical vein endothelial cell (HUVEC) cultures after 4 hours exposure to IL-33 or IL-1M-NM-2. Analysis of these data revealed a striking similarity in the transcriptional response to the two cytokines. Pooled HUVEC from 10 donors were seeded 10.000 cells/cm2 and cultured for 4 days before stimulation for 4 hours with IL-1M-NM-2 0.5 ng/ml or IL-33 50 ng/ml. Total RNA was isolated using the RNeasy Mini Kit (Qiagen) according to instructions of the manufacturer. Microarrays were performed using an Illumina Human6 v2 Expression Beadchip, and the raw data was pre-processed by IlluminaM-bM-^@M-^Ys BeadStudio software V2. The expression service was provided by Helse SM-CM-8r-M-CM-^Xst/University of Oslo Microarray Core Facility, a member of the Norwegian Microarray Consortium supported by the functional genomics program (FUGE) at the Research Council of Norway.

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Interleukin-33 contributes to anemia of chronic inflammation by inhibiting differentiation of erythroid progenitors

Project description:Mature blood cells are produced continuously from hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM). During chronic inflammation, this process may be perturbed by inflammatory cytokines acting on HSPCs to cause anemia of inflammatory disease. Among BM HSPCs, we found the receptor for interleukin (IL)-33, ST2, was expressed preferentially and highly on erythroid progenitors. Induction of inflammatory spondyloarthritis in mice increased IL-33 in BM plasma, and IL-33 was required for inflammation-dependent suppression of erythropoiesis in BM. Conversely, administration of IL-33 in healthy mice suppressed erythropoiesis, decreased hemoglobin expression, and caused anemia. Using purified erythroid progenitors in vitro, we showed that IL-33 directly inhibited terminal maturation. This effect was dependent on NF-kB activation and was associated with altered signalling events downstream of the erythropoietin receptor. Accordingly, IL-33 also suppressed erythropoietin-induced stress erythropoiesis in vivo. These results reveal a role for IL-33 in regulation of erythropoiesis during inflammatory disease and define a new target for its treatment.

2020-05-15 | GSE141480 | GEO

Microarray analysis of human cord blood derived mast cells (hCBMC) activated by Interleukin-33 (IL-33)

Project description:Mast cells respond to acute and chronic exposure to IL-33 by differing the expression of their receptors, cytokines and proteases. We aim to characterize the distinct acute and chronic responses of mast cells to IL-33 by analyzing hCBMC expression profile of pro- and anti- inflammatory mediators.

2024-10-03 | GSE224089 | GEO

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Glioma cells response Interleukin-33 (IL-33) [microarray]

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Expression data from endothelial cells isolated from IL-33 knock-out and wildtype rats

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2023-12-31 | GSE121577 | GEO

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