Antagonizing IL-1β to treat GBM
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA824138 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18669228_1.fastq.gz | Fastqsanger.gz | |||
| SRR18669228_2.fastq.gz | Fastqsanger.gz | |||
| SRR18669229_1.fastq.gz | Fastqsanger.gz | |||
| SRR18669229_2.fastq.gz | Fastqsanger.gz | |||
| SRR18669230_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 72 |
Similar Datasets
Project description:Monocytes and monocyte-derived macrophages (MDM) from blood circulation infiltrate and promote glioblastoma growth by, at least partially, expressing pro-inflammatory cytokine IL-1β . Using SC-RNA seq, we analyze how IL1a and IL1b differentially contibute to tumor growth.
2023-10-13 | GSE200348 | GEO
Project description:Toll-like receptors/Interleukin-1 receptor (IL-1R) signaling plays an important role in High-fat diet (HFD)-induced adipose tissue dysfunction contributing to obesity-associated metabolic syndromes. Here, we show an unconventional IL-1R-IRAKM (IL-1R-associated kinase M)-Slc25a1 signaling axis in adipocytes that reprograms lipogenesis to promote diet-induced obesity. Adipocyte-specific deficiency of IRAKM reduced HFD-induced body weight gain, increased whole body energy expenditure and improved insulin resistance, associated with decreased lipid accumulation and adipocyte cell sizes. IL-1β stimulation induced the translocation of IRAKM Myddosome to mitochondria to promote de novo lipogenesis in adipocytes. Mechanistically, IRAKM interacts with and phosphorylates mitochondrial citrate carrier Slc25a1 to promote IL-1β-induced mitochondrial citrate transport to cytosol and de novo lipogenesis. Moreover, IRAKM-Slc25a1 axis mediates IL-1β induced Pgc1a acetylation to regulate thermogenic gene expression in adipocytes. IRAKM kinase-inactivation also attenuated HFD-induced obesity. Taken together, our study suggests that the IL-1R-IRAKM-Slc25a1 signaling axis tightly links inflammation and adipocyte metabolism, indicating a novel therapeutic target for obesity.
2022-06-09 | PXD031934 | Pride
Project description:Interleukin-1 (IL-1) is a key pro-inflammatory cytokine, which has diverse actions in the brain as a regulator of host defence responses and a mediator of inflammation. Two major agonists, IL-1α and IL-1β bind to a single known functional (type-1) IL-1 receptor (IL-1RI), which associates with an accessory protein (IL-1RAcP) leading to signal transduction. However, recent evidence suggests that some actions of IL-1 in the brain may be independent of IL-1R1 and its classical signalling pathways, pointing to an as yet unidentified functional receptor for IL-1 expressed in the CNS. In this study, cDNA array based gene expression profiling was used to identify possible genes induced by IL-1β independently of IL-1R1. The results show that IL-1β may indeed regulate some genes independently of IL-1R1, suggesting the presence of additional functional IL-1 receptors in the mouse brain. Keywords: experimental treatment (IL-1β), gene ablation (IL-1R1), glia
2006-03-25 | GSE4507 | GEO
Project description:The canonical pathway for IL-1β production requires TLR-mediated NF-κB-dependent Il1b gene induction, followed by caspase-containing inflammasome-mediated processing of pro-IL-1β. Here we show that IL-21 unexpectedly induces IL-1β production in conventional dendritic cells (cDCs) via a STAT3-dependent but NF-κB-independent pathway. IL-21 does not induce Il1b expression in CD4+ T cells, with differential histone marks present in these cells versus cDCs. IL-21-induced IL-1β processing in cDCs does not require caspase-1 or caspase-8 but depends on IL-21-mediated death and activation of serine protease(s). Moreover, STAT3-dependent IL-1β expression in cDCs at least partially explains the IL-21-mediated pathologic response occurring during infection with Pneumonia Virus of Mice. These results demonstrate lineage-restricted IL-21-induced IL-1β via a non-canonical pathway and provide evidence for its importance in vivo.
2015-07-07 | GSE61677 | GEO
Project description:To gain a better understanding of the role of Interleukin-1β (IL-1β) in lung CD140a+ mesenchymal cells (fibroblasts) modulation, we performed RNA-seq to compare the transcriptomes of IL-1β-treated and control lung CD140a+ mesenchymal cells (fibroblasts).
2022-07-19 | E-MTAB-11887 | biostudies-arrayexpress
Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. Human islets were isolated and exposed (or not) to IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix arrays. These measurements were performed three times.
2013-12-19 | E-GEOD-53454 | biostudies-arrayexpress
Project description:Serine is a substrate for nucleotides, NADPH and glutathione (GSH) synthesis. Previous studies in cancer cells and lymphocytes have shown that serine-dependent one-carbon units are necessary for nucleotide production to support proliferation. Presently, it is unknown whether serine metabolism impacts the function of non-proliferative cells, such as inflammatory macrophages. We find that in macrophages, serine is required for optimal lipopolysaccharide (LPS) induction of IL-1β mRNA expression, but not inflammasome activation. The mechanism involves a requirement for glycine, which is made from serine, to support macrophage glutathione (GSH) synthesis. Cell-permeable GSH, but not the one-carbon donor formate, rescues IL-1β mRNA expression. Pharmacological inhibition of de novo serine synthesis in vivo decreased LPS induction of IL-1β levels and improved survival in an LPS-driven model of sepsis in mice. Our study reveals that serine metabolism is necessary for GSH synthesis to support IL-1β cytokine production.
2019-01-15 | GSE125036 | GEO
Project description:The conditioned media from Bifidobacterium infantis (BCM) and Lactobacillus acidophilus (LCM) were reported to promote maturation of innate immune response gene expression, which explained the protective effects of probiotics in clinical necrotizing enterocolitis. We used microarray analysis to investigate the expression of genes involved in regulation of BCM and LCM in IL-1β stimulated immature human enterocytes. The H4 cells (a human nontransformed primary intestinal epithelial cell line) were pretreated with BCM or LCM (15%) for 30 minutes, and then stimulated with or without IL-1β (10 ng/mL) for 4 h. Cell media and IL-1β stimulation were negative and positive control, respectively. RNA was extracted for mcroarray analysis. A total of six treatments (triplicates for each) were included in this study. As one RNA sample in IL-1β-stimulated cells treated with BCM was dropped due to bad quality, seventeen samples were analyzed. Various treatments were compared to the nagative control (cell media alone). Genes with a fold-change ≥2 and a p value ≤ 0.05 were selected.
2015-06-22 | E-GEOD-62208 | biostudies-arrayexpress
Project description:Serine metabolism supports macrophage IL-1β production.
| PRJNA515004 | ENA
Project description:Mesenchymal stem cells are often transplanted in inflammatory environments and they are able to survive and modulate host immune responses through mechanism poorly understood. In this paper we analyzed biological responses of MSC in response IL-1β as a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activates a set of biological process related with cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of immune response. Further analysis by real-time PCR and functional assays revealed that IL-1β mainly increases production of chemokines CCL5, CCL20, CXCL1, CXCL3, CXCL5, CXCL6, CXCL10, CXCL11 and CX3CL1, interleukins IL-6, IL-8, IL23A, IL32, Toll-like receptors TLR2, TLR4, CLDN1, metalloproteins MMP1 and MMP3, growth factors CSF2 and TNF, together with adhesion molecules ICAM1 and ICAM4. Functional analysis of MSC proliferation, migration and adhesion to extracellular matrix components revealed that IL-1β did not affect proliferation whereas constitute a throphic factor for MSC and increases adhesion mainly to collagen and laminin. Moreover, IL-1β treatment enhanced the ability of MSC to recruit monocytes and granulocytes cells in vitro. Blockade of NFkβ transcription factor activation with IκB kinase beta (IKKb) siRNA impaired MSC migration, adhesion and leucocyte recruitment, indicating that NF-kB signaling pathway is the main mechanism implicated in these biological processes. These findings are relevant for designing protocols that implicate MSC delivery into inflammatory environments.
2012-06-22 | GSE33755 | GEO