Ontology highlight
ABSTRACT:
PROVIDER: PRJNA368966 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5218300.fastq.gz | Fastqsanger.gz | |||
| SRR5218310.fastq.gz | Fastqsanger.gz | |||
| SRR5218320.fastq.gz | Fastqsanger.gz | |||
| SRR5218330.fastq.gz | Fastqsanger.gz | |||
| SRR5218340.fastq.gz | Fastqsanger.gz |
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Project description:Comparative colonic mucosal transcriptomics of 10 patients with PSC-IBD, 10 UC and 10 Healthy controls
2019-09-01 | E-MTAB-7915 | biostudies-arrayexpress
Project description:Primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and inflammatory bowel diseases (IBDs), including Crohn’s disease (CD) and ulcerative colitis (UC), are heterogeneous chronic autoimmune diseases that may share underlying pathogenic mechanisms. Herein, we compared simultaneously analyzed blood transcriptomes from patients with PBC, PSC, and IBD.
2019-05-01 | GSE119600 | GEO
Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.
2015-10-10 | GSE73882 | GEO
Project description:Background: Patients suffering from primary sclerosing cholangitis (PSC) often also have ulcerative colitis (UC). Cross-disease genetic and microbiome studies across PSC und UC patients indicated that UC in PSC is a separate disease entity from primary UC, but expression studies for PSC are lacking. In this study, we performed a molecular comparison of whole blood expression levels in PSC only, PSC patients with additional UC diagnosis (PSC/UC), and UC, using a large collection of whole blood transcriptome data. Methods: We conducted whole blood RNA-Seq experiments for 495 UC patients, 220 PSC patients (of whom 177 have also a UC diagnosis), and 320 healthy controls from Germany and Norway. Differential expression analyses, gene ontology and coexpression analyses and random forest machine learning were performed to identify genes, ontologies and transcriptional features that discriminate diagnoses. Results: The blood transcriptome in UC and PSC is dominated by neutrophil activation genes. In UC, but not in PSC (neither PSC alone nor PSC/UC), there is upregulation of genes for ribosomes, mitochondria and energy metabolism genes in conjunction with antibody transcript expression. In PSC, there is an increase in modules related to apoptosis and expression of genes of interferon-I-related ontologies. Random forest analysis could poorly discriminate PSC alone from PSC/UC (AUROC 0.56), but could discriminate PSC, UC, and controls with high accuracy (AUROC UC vs controls 0.95, PSC vs controls 0.88, UC vs PSC 0.986). The main coexpression modules are enriched in neutrophil degranulation and antibody production genes relevant for distinguishing PSC, UC, and controls. Conclusions: PSC and UC share neutrophil-related transcriptional upregulation in whole blood (e.g. S100A12). UC is characterised by upregulation of modules involved in antibody production (MZB1, IGJ) and increased metabolic activity (PDK4, ribosomal genes), while PSC differs from UC by interferon (IFIT1) and apoptosis upregulation (G0S2). Supported by machine learning results, PSC and UC are interpreted as molecularly separate entities, while PSC/UC and PSC are indistinguishable.
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Project description:Defects in RNA splicing have been linked to numerous human disorders, but remain poorly explored in inflammatory bowel disease (IBD). Here, we report that, in the gut epithelium of patients with ulcerative colitis (UC), the expression of the chromatin and alternative splicing regulator HP1g is strongly reduced. Accordingly, inactivation of the HP1g gene in the mouse gut triggered several IBD-like traits, including inflammation and dysbiosis. In parallel, we discovered that its loss of function broadly increased splicing noise, reducing requirement for canonical splicing consensus sequences, and favoring the usage of cryptic splice sites at numerous genes with key functions in gut biology. This notably resulted in the production of progerin, a noncanonical toxic splice variant of prelamin A mRNA, responsible for the Hutchinson Gilford Progeria Syndrome (HGPS) of premature aging. Likewise, production of progerin transcript was found to be a signature of colonic cells from UC patients. Thus, our study identifies HP1g as a regulator of RNA metabolism in vivo, providing a unique mechanism linking anti-inflammation and accuracy of RNA splicing in the gut epithelium. HP1 defect may confer a general disturbance in RNA splicing precision to scrutinize in IBD and more generally in accelerating aging diseases.
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Project description:Significant gut microbiota heterogeneity exists amongst UC patients though the clinical implications of this variance are unknown. European and South Asian UC patients exhibit distinct disease risk alleles, many of which regulate immune function and relate to variation in gut microbiota β-diversity. We hypothesized ethnically distinct UC patients exhibit discrete gut microbiotas with unique luminal metabolic programming that influence adaptive immune responses and relate to clinical status. Using parallel bacterial 16S rRNA and fungal ITS2 sequencing of fecal samples (UC n=30; healthy n=13), we corroborated previous observations of UC-associated depletion of bacterial diversity and demonstrated significant gastrointestinal expansion of Saccharomycetales as a novel UC characteristic. We identified four distinct microbial community states (MCS 1-4), confirmed their existence using microbiota data from an independent UC cohort, and show they co-associate with patient ethnicity and degree of disease severity. Each MCS was predicted to be uniquely enriched for specific amino acid, carbohydrate, and lipid metabolism pathways and exhibited significant luminal enrichment of metabolic products from these pathways. Using a novel in vitro human DC/T-cell assay we show that DC exposure to patient fecal water led to MCS -specific changes in T-cell populations, particularly the Th1:Th2 ratio, and that patients with the most severe disease exhibited the greatest Th2 skewing. Thus, based on ethnicity, microbiome composition, and associated metabolic dysfunction, UC patients may be stratified in a clinically and immunologically meaningful manner, providing a platform for the development of FMC-focused therapy. Fecal microbiome was assessed with Affymetrix PhyloChip arrays from patients with ulcerative colitis and healthy controls.
2016-07-25 | E-GEOD-78724 | biostudies-arrayexpress
Project description:Activation of inflammatory pathways in human IBD IL-6:STAT3 pathways are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory IL-6:STAT3 dependent networks would be up regulated in the colon of pediatric patients with Crohn Disease (CD) and Ulcerative Colitis (UC), and that these would regulate leukocyte survival, proliferation, and recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy, CD, and UC samples. Colon biopsy samples were obtained from CD and UC patients at diagnosis, CD patients during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that two IL-6:STAT3 dependent networks are up regulated in pediatric IBD both at diagnosis and during therapy which regulate leukocyte recruitment and survival. The degree of up regulation of these genes compared to healthy controls was remarkably conserved across the two CD groups and the UC groups, suggesting common mechanisms of mucosal inflammation. Colon RNA was isolated from biopsies obtained from CD at diagnosis and during therapy, UC at diagnosis, and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1-4) used for normalization of the Sample VALUEs are linked below as supplementary files.
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Project description:Primary sclerosing cholangitis (PSC) is an autoimmune-like disease of the bile ducts that co-occurs with inflammatory bowel disease (IBD) in almost 90% of cases. Colorectal cancer is a major complication of patients with both PSC and IBD, and these patients are at a much greater risk compared to patients with IBD without concomitant PSC. Combining flow cytometry, bulk and single cell transcriptomics, and T- and B-cell receptor repertoire analysis of right colon tissue from PSC, IBD, and healthy controls we identified a unique adaptive inflammatory transcriptional signature associated with greater risk and shorter time to dysplasia specifically in patients with PSC. This inflammatory signature is characterized by antigen-driven IL-17A+ Foxp3+ CD4 T-cell and an expansion of IgG-secreting B-cell responses. These data results suggest that the mechanisms that drive the emergence of dysplasia in of PSC and IBD dysplasia are distinct and provide molecular insights to guide prevention of colorectal cancer in PSC.
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