EGAS00001001590-sc-20160629 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001002233 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:RNA sequencing of peripheral immune cells from patients +/- an IBD risk variant. Peripheral immune cells +/- in vitro test compound treatment.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2016-07-11 | E-ERAD-443 | biostudies-arrayexpress
Project description:RNA sequencing of peripheral immune cells from patients +/- an IBD risk variant. Peripheral immune cells +/- in vitro test compound treatment.
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAS00001001590 | EGA
Project description:RNA sequencing of peripheral immune cells from patients +/- an IBD risk variant. Peripheral immune cells +/- in vitro test compound treatment.
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ .
This dataset contains all the data available for this study on 2019-02-15.
| EGAD00001004777 | EGA
Project description:Presenting features of inflammatory bowel disease (IBD) are non-specific. We hypothesized that mRNA profiles could (1) identify genes and pathways involved in disease pathogenesis; (2) identify a molecular signature that differentiates IBD from other conditions; (3) provide insight into systemic and colon-specific dysregulation through study of the concordance of the gene expression. Children (8-18 years) were prospectively recruited at the time of diagnostic colonoscopy for possible IBD. We used transcriptome-wide mRNA profiling to study gene expression in colon biopsies and paired whole blood samples. Using blood mRNA measurements, we fit a regression model for disease state prediction that was validated in an independent test set of adult subjects (GSE3365). Results: Ninety-eight children were recruited [39 Crohn’s disease, 18 ulcerative colitis, 2 IBDU, 39 non-IBD]. There were 1,118 significantly differentially (IBD vs non-IBD) expressed genes in colon tissue, and 880 in blood. The direction of relative change in expression was concordant for 106/112 genes differentially expressed in both tissue types. The regression model from the blood mRNA measurements distinguished IBD vs non-IBD disease status in the independent test set with 80% accuracy using only 6 genes. The overlap of 5 immune and metabolic pathways in the two tissue types was significant (p<0.001). Conclusions: Blood and colon tissue from patients with IBD share a common transcriptional profile dominated by immune and metabolic pathways. Our results suggest that peripheral blood expression levels of as few as 6 genes (IL7R, UBB, TXNIP, S100A8, ALAS2, and SLC2A3) may distinguish patients with IBD from non-IBD. Ninety-eight children were recruited [39 Crohn’s disease, 18 ulcerative colitis, 2 IBDU, 39 non-IBD]. There were 1,118 significantly differentially (IBD vs non-IBD) expressed genes in colon tissue, and 880 in blood. The direction of relative change in expression was concordant for 106/112 genes differentially expressed in both tissue types. The regression model from the blood mRNA measurements distinguished IBD vs non-IBD disease status in the independent test set with 80% accuracy using only 6 genes. The overlap of 5 immune and metabolic pathways in the two tissue types was significant (p<0.001). Conclusions: Blood and colon tissue from patients with IBD share a common transcriptional profile dominated by immune and metabolic pathways. Our results suggest that peripheral blood expression levels of as few as 6 genes (IL7R, UBB, TXNIP, S100A8, ALAS2, and SLC2A3) may distinguish patients with IBD from non-IBD.
2019-10-29 | GSE126124 | GEO
Project description:The aim of the study is to characterize in vitro PGC methylation dynamics and study effects of modualting epigenetic regulators.Germ cells were derived in vitro, and PBAT libraries were generated according to internal developed protocolsThis data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-03-24 | E-ERAD-345 | biostudies-arrayexpress
Project description:This study involves targeted sequencing of samples from myeloid malignancies at different timepoints to assess clonal evolution of malignancy
a. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAD00001002225 | EGA
Project description:Inflammatory bowel disease (IBD) is characterized by chronic mucosal inflammation of the gastrointestinal tract and is associated with extracellular acidification of mucosal tissue. Several extracellular pH-sensing receptors, including G protein-coupled receptor 4 (GPR4), play an important role in the regulation of inflammatory and immune responses and GPR4 deficiency has been shown to be protective in IBD animal models. To confirm the therapeutic potential of GPR4 antagonism in IBD, we tested Compound 13, a selective GPR4 antagonist, in the IL10-/- mouse model of colitis. Despite reasonable bioavailability, Compound 13 treatment did not improve colitis in this model and there were no signs of target engagement. Interestingly, Compound 13 behaved as an “orthosteric” antagonist, i.e., its potency was pH-dependent and mostly inactive at pH levels lower than 6.8 with preferential binding to the inactive conformation of GPR4. Mutagenesis studies confirmed Compound 13 likely binds to the conserved orthosteric binding site in G protein-coupled receptors, where a histidine sits in GPR4 likely preventing Compound 13 binding when protonated in acidic conditions. While the exact mucosal pH in the human disease and relevant IBD mice models is unknown, it is well established that the degree of acidosis is positively correlated with the degree of inflammation, suggesting Compound 13 is not an ideal tool to study the role of GPR4 in moderate-to-severe inflammatory conditions.
2024-01-03 | GSE225694 | GEO
Project description:Patient-derived xenografts (n=96) were derived from metastatic melanoma patients. RNA expression profiling will be preformed to study 1. HLA-typing and 2. the effect of the tumour microenvironment on tumour growth
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAD00001002230 | EGA
Project description:Clinical remission is apparent when laboratory markers of inflammation are normal and clinical symptoms are absent. However, sub-clinical inflammation can still be present. A detailed analysis of the immune status during this inactive state of disease may provide a useful tool to subcategorize patients with subclinical immune activation We performed (un)supervised clustering analysis of IBD-associated genes and applied IngenuityM-BM-. pathway software to identify specific molecular profiles between patients. We analyzed RNA gene expression profiles of peripheral blood leucocytes (PBL) from pediatric IBD patients in clinical remission and age-matched controls.
2013-10-04 | E-GEOD-33943 | biostudies-arrayexpress
Project description:<p>Pre-IBD is a transitional state between irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), in which chronic high-fat diet intake and antibiotic exposure significantly increase intestinal inflammatory susceptibility. However, the underlying mechanisms and effective therapeutic strategies remain inadequately understood. Milk-derived extracellular vesicles (mEVs) have emerged as promising nanotherapeutic agents for alleviating gut disorders. In this study, we found that pre-IBD mice exhibited profound gut microbiota dysbiosis, and treatment with mEVs significantly alleviated intestinal inflammation by modulating MAPK-mediated M1/M2 macrophage polarization and restoring microbiota balance. Mechanistically, mEVs treatment led to a reduction in lysophosphatidylcholine (LPC) levels and an enrichment of Lactobacillus murinus (L. murinus), which exerted opposing effects on intestinal inflammation in both in vivo and in vitro models. Specifically, LPC exacerbated intestinal inflammation and structural alterations, whereas L. murinus treatment mitigated these pathological changes. Notably, both LPC and L. murinus interact with TLR2 but activate distinct downstream signaling pathways. LPC activates the TLR2/MAPK/NF-κB axis, promoting M1 polarization, whereas L. murinus binding to TLR2 induces M2 polarization. These findings demonstrate that mEVs reprogram the TLR2-mediated immune response by modulating the levels of L. murinus and LPC, thereby mitigating gut inflammation and contributing to the attenuation of pre-IBD pathology.</p>
2026-04-29 | MTBLS14399 | MetaboLights