PSC-IBD mucosal biology
Ontology highlight
ABSTRACT:
INSTRUMENT(S): NextSeq 550
ORGANISM(S): Homo sapiens
SUBMITTER: Mohammed Nabil Quraishi
PROVIDER: E-MTAB-7915 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:'Illumina Infinium HumanMethylation450 BeadChip data from CD326+ sorted colonic epithelial cells of mucosal biopsies from treatment-naive paediatric IBD patients (Crohn''s Disease or Ulcerative Colitis) or age-matched controls AC= ascending colon, PSC=sigmoid colon'
2015-09-15 | E-MTAB-3709 | biostudies-arrayexpress
Project description:Rationale: Ulcerative colitis (UC) is characterized by colonic mucosal inflammation and barrier dysfunction. We hypothesize that UC causes persistent defects in mucosal homeostasis, evident even in the absence of inflammation, contributing to disease chronicity. Objective: To test this, we grew patient biopsy-derived sigmoid colonoids into air-liquid interface (ALI) monolayers, characterizing them through microscopy, proteomics, bulk RNAseq, and their susceptibility to UC patient-isolated Escherichia coli pathobiont p19A. Findings: Non-IBD ALI monolayers formed uniform crypt-like structures, mature goblet cells and a thick mucus layer containing all epithelial-derived proteins previously identified in human colonic mucus. In contrast, ALI monolayers from UC patients displayed a range of impairments, from distorted crypt-like structures and a thinner and more permeable mucus layer to severe defects in cellular differentiation and crypt development. Transcriptome analysis identified activated pathways associated with extracellular matrix formation and cell signaling, including numerous cancer-associated genes in UC ALI monolayers, which also proved significantly more susceptible to E. coli p19A. Conclusions: The culturing of patient biopsies into ALI colonoid monolayers provides a powerful model to assess human mucosal development, healing, homeostasis and mucus barrier function, revealing that UC-derived colonoids display a range of developmental and functional defects that persist in the absence of inflammation.
2026-01-29 | PXD064643 | Pride
Project description:Background: The Inflammatory Bowel Disease (IBD) ulcerative colitis (UC) is characterized by colonic mucosal inflammation and barrier dysfunction. We hypothesize that UC causes persistent defects in mucosal homeostasis, evident even in the absence of active inflammation, contributing to disease chronicity. Methods: To test this, we grew patient biopsy-derived sigmoid colonoids into air-liquid interface (ALI) monolayers, characterizing them through microscopy, proteomics, bulk RNAseq, and their susceptibility to UC patient-isolated Escherichia coli pathobiont p19A. Results: Non-IBD ALI monolayers formed uniform crypt-like structures and a thick mucus layer containing all epithelial-derived proteins previously identified in human colonic mucus. In contrast, ALI monolayers from UC patients displayed a range of impairments, classified as a mild phenotype with distorted architecture and a thinner, more permeable mucus layer to a severe phenotype with defects in cellular differentiation and an inability to produce a mucus layer. Transcriptome analysis identified activated pathways associated with extracellular matrix formation and cell signaling, including numerous cancer-associated genes in UC ALI monolayers, which also proved significantly more susceptible to E. coli p19A. Conclusions: Taken together, the culturing of patient biopsies into ALI colonoid monolayers provides a powerful model to assess human colonic mucosal development, healing, homeostasis, and mucus barrier function, revealing that UC-derived colonoid monolayers display a range of developmental and functional defects that persist in the absence of inflammation.
2026-01-29 | GSE299477 | GEO
Project description:Background & Aims: Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state. Methods: Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and with irritable bowel syndrome (controls, n=10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden). Results: A clear separation between active UC, quiescent UC and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines revealing a plausible explanation to the abnormal regulated innate immune response seen in patients with UC. Conclusion: This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Keywords: Colonocytes, continuous inflammation, mucosal colonic biopsies, gene expression profiles Adjacent mucosal colonic biopsies were attained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and in controls (n=10). After extraction of total RNA, genome-wide gene expression data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Amplification was required to obtain sufficient amounts of labelled complementary RNA (cRNA) target for analysis with arrays. Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden).
2009-09-16 | E-GEOD-13367 | biostudies-arrayexpress
Project description:Peripheral blood-derived macrophages were stimulated with viral-like particles isolated from colonic resections from patients with Crohn's disease (CD), ulcerative colitis (UC), or non-IBD controls diagnoses. RNAseq was performed to unbiasedly assess the transcriptional responses to these stimuli and revealed highly divergent macrophage transcriptional programs in response to non-IBD compared to IBD VLP.
2020-06-01 | GSE135223 | GEO
Project description:Background & Aims: Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state. Methods: Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and with irritable bowel syndrome (controls, n=10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden). Results: A clear separation between active UC, quiescent UC and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines revealing a plausible explanation to the abnormal regulated innate immune response seen in patients with UC. Conclusion: This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Keywords: Colonocytes, continuous inflammation, mucosal colonic biopsies, gene expression profiles
2009-09-16 | GSE13367 | GEO
Project description:Differential diagnosis in inflammatory bowel disease (IBD) patients from the start of the diagnosis is challenging. In this study we tried to discriminate two subtypes of IBD such as Chron's disease(CD) and Ulcerative colitis (UC) using differential expression of genes from formalin-fixed paraffin-embedded mucosal biopsies of 33 IBD patients and 10 healthy controls.
2023-10-27 | GSE222070 | GEO
Project description:Background: Primary sclerosing cholangitis (PSC) is a progressive cholestatic disease with up to 80% of patients also suffering from ulcerative colitis (PSC-UC). The difficulty in the diagnosis along with the increased risk for developing cancer represent a clinical challenge. Furthermore, the precise molecular factors regulating the phenotype of this disease subtype remain unknown. Methods: We applied methyl-capture sequencing and mRNA sequencing to colonic mucosal biopsies from 3 groups of treatment-naïve children at diagnosis from the DOCHAS study - UC (n=10), PSC-UC (n=10) and healthy controls(n=10). Results: Differential gene expression between UC and PSC-UC identified disease-associated genes that were either up- or down-regulated in UC or PSC relative to controls. Specifically, expression of these genes was regulated by master transcriptional regulators (pro-caspases, IL7RA) and transcription factors (AR, p53, JUND, CEBPA). Importantly, gene expression comparison between UC vs PSC-UC revealed 4 up- and 4 down-regulated genes in PSC-UC patients. Notably, RAB31 and TENM3 identified as upregulated in the PSC-UC patients, are also significantly up-regulated in gastrointestinal (GI) cancers. Differential methylation analysis between controls biopsies vs PSC-UC and UC demonstrated >1000 differentially methylated regions (DMRs) with a large proportion of these DMRs enriched in enhancer regions. Conclusion: Our study, for the first time, identifies distinct gene expression and DNA methylation alterations that differentiate UC from PSC-UC at diagnosis in treatment-naïve paediatric patients, some of which are associated with GI cancers. These findings suggest the potential utility of these molecular markers as predictive biomarkers for PSC development in UC or for assessing dysplasia risk in PSC-UC. Further validation in larger patient cohorts is warranted.
2026-01-31 | GSE283289 | GEO