Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263475 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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.
2015-06-22 | GSE62208 | GEO
Project description:Investigating transcriptional profile of WT and LKB1 knockout mouse embryonic fibroblasts untreated, stimulated with IL-1β, treated with A485 alone, or stimulated with IL-1β and A485
2023-05-11 | GSE227446 | GEO
Project description:Pulmonary metastasis is a major cause of mortality in colorectal cancer (CRC), and the tumor microenvironment plays a critical role in metastatic progression. In particular, inflammatory fibroblasts have been implicated in shaping the metastatic niche; however, the molecular characteristics of their extracellular vesicles (EVs) remain incompletely understood. In this study, we performed LC-MS/MS-based proteomic analysis of EVs derived from IL-1β–stimulated MRC-5 lung fibroblasts. EVs were isolated from conditioned media of MRC-5 cells with or without IL-1β treatment and subjected to comparative proteomic profiling. This dataset provides a resource for characterizing EV-associated protein alterations in inflammatory fibroblasts and supports further investigation of their potential roles in tumor-related processes in colorectal cancer lung metastasis.
2026-03-20 | PXD075933 |
Project description:To study differentially expressed genes via RNA seq analysis of CD8+T-cells from C57BL/6 mice splenocytes treated with the four different conditions: IL-2, IL-2 80%TCM, IL-12 and IL-12 80%TCM. (TCM = Tumor Conditioned Media)
2021-11-23 | GSE189170 | GEO
Project description:We report the differential mRNA expression of memory-like CD4+ T cells stimulated with iL-7, IL-1β, and IL-23. We found memory-like CD4+ T cells stimulated with IL-1β, or with IL-1β and IL-23, in the presence of IL-7, displayed a unique gene expression signature.
2019-02-26 | GSE124045 | GEO
Project description:Invasive Lobular Carcinoma (ILC) is an under-studied yet common subtype of breast cancer. A key feature of ILC tumours, due to their single-file invasive growth pattern, is a high stromal content and in particular, an abundance of cancer-associated fibroblasts (CAFs). We identified that IL-6 secreted from primary ILC patient-derived CAFs drives STAT3 activation in ILC cell lines and found that IL6, STAT3, pSTAT3 and subsequent downstream gene expression induced by IL-6 within CAF conditioned media is upregulated in ILC tumours compared to Invasive Ductal Carcinoma tumours, the most common subtype of breast cancer. This dataset contains 3`-mRNAseq data from ILC cell lines (SUM44PE and MDA-MB-134VI) and patient-derived organoids (HCI-013 and HCI-018) stimulated with either recombinant human IL-6 (10 ng/ml) for 24 hours or 1 week or SUM44PE cells stimulated with CAF conditioned media (CAF CM)collected from ED26 primary ILC CAFs (characterised here: doi.org/10.3390/cancers14040904) +/- an IL-6 neutralising antibody. RNA was extracted using Qiagen RNeasy mini-kit and libraries were prepared using QuantSeq 3’ mRNA-Seq Library Prep Kit (FWD) for Illumina (Lexogen Inc, #015).
2024-10-11 | GSE276108 | GEO
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
Project description:Palmitic acid (PA) absorption from the intestine is increased in metabolic dysfunction-associated steatohepatitis (MASH). It induces endoplasmic reticulum (ER) stress and interleukin-1 beta (IL-1β) production in hepatic stellate cells (HSCs). Protein kinase R-like endoplasmic reticulum kinase (PERK) is an ER stress sensor protein involved in HSC activation and liver fibrosis. However, its role in HSCs during hepatocellular carcinoma (HCC) progression remains unclear. This study clarified the process of IL-1β production via PERK in HSCs and explored the mechanism underlying MASH-related HCC progression. HSCs were treated with PA or transfected with PERK small-interfering RNA (siRNA) or PERK plasmid. Proliferation, scratch, and Transwell assays were performed on HCC cells cultured in the conditioned medium (CM) from HSCs. PA treatment increased PERK and IL-1β expressions in HSCs. PERK knockdown decreased IL-1β expression, while its overexpression increased it in HSCs. The CM from PA-treated HSCs showed elevated IL-1β levels and enhanced HCC cells’ proliferation, migration, and invasion; however, these effects were suppressed by PERK knockdown in HSCs. RNA-sequencing analysis revealed that p38δ mitogen-activated protein kinase (MAPK) is the intermediate molecule between PERK and IL-1β in HSCs. In the tumor microenvironment of MASH-related HCC, PERK in HSCs promotes HCC progression via the p38δ MAPK/IL-1β axis.
2025-06-07 | GSE292002 | GEO
Project description:Backgrounds: During atherogenesis, macrophages turn into foam cells by engulfing lipids present within the atheroma plaques. The shift of foam cells towardspro- or anti-inflammatory phenotypes, critical step in disease progression, is still poorly understood. Liver X Receptors (LXRs) play a pivotal role in the macrophage response to lipid, promoting the expression of key genes of cholesterol efflux, mitigating intracellular cholesterol accumulation. LXRs also exert balanced actions on inflammation in human macrophages, displaying both pro- and anti-inflammatory effects. Aims and methods: Our study explored the role of LXRs in the functional response of human macrophage to lipid-rich plaque environment. We used primary human macrophages treated with atheroma plaque extracts and assessed the impact of pharmacological LXR inhibition by GSK2033 on cholesterol homeostasis and inflammatory response. Ultimately, we evaluated macrophage and endothelial cell crosstalk by assessing the impact of macrophage-conditioned supernatants on human endothelial cell. Results: LXR inhibition by GSK2033 resulted in increased levels of cholesterol and oxysterols in human macrophages, alongside notable changes in the cholesterol ester profile. This was accompanied by heightened secretion of pro-inflammatory cytokines such as IL-6 and TNFα, despite a transcriptional repression of IL-1β. Conditioned media from GSK2033-treated macrophages more effectively activated ICAM-1 and CCL2 expression in endothelial cells. Conclusions/perspectives: Our findings illustrate the intricate relationship between LXR function, cholesterol metabolism, and inflammation in human macrophages. While LXR is required for the proper handling of plaque lipids by macrophages, the differential regulation of IL-1β versus IL-6/TNFα secretion by LXRs could be challenging for potential pharmacological interventions.
2026-03-19 | GSE292423 | GEO