E-TABM-176
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ABSTRACT:
PROVIDER: E-TABM-176 | ExpressionAtlas | 2015-11-02
REPOSITORIES: ExpressionAtlas
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Project description:Irritable bowel syndrome (IBS) is a highly prevalent disorder of the gastrointestinal tract characterized by abdominal pain, bloating, and disturbed bowel function. Here we report on the analysis of microarray expression profiles of sigmoid colon mucosal biopsies from IBS patients and healthy control subjects. Two samples were collected from each individual. From 10 individuals, a third sample was collected 2-3 months after the initial collection. The repeat samples were used to assess the robustness of the expression profiles over different locations within the colon and over time. This analysis revealed a number of differentially expressed genes in IBS patients, which point to functional alterations of specific components of the host defence system and the immune response. This is in support of an important role for peripheral gastrointestinal changes underlying the aetiology of IBS. Two gene probe sets with the most strikingly increased expression in mucosal colon biopsies of IBS patients represent a gene that is, as yet, uncharacterised (DKFZP564O0823). We propose to rename this gene IBS1. We also report on the identification of specific sets of gene probes on the microarray, so-called molecular signatures, which enable the distinction of IBS patients from healthy controls. The expression profiles in IBS are consistent across different sites within the sigmoid colon and are stable over time.
2007-11-24 | E-TABM-176 | biostudies-arrayexpress
Project description:Hypothesis: Gene expression differences in biopsies from patients with inflammatory bowel disease can be used to identify molecular heterogeneity within patients with active disease. Methods: Patients with a diagnosis of Crohn's disease, ulcerative colitis or normal healthy controls (with or without infectious colitis) underwent ileocolonoscopy. In healthy controls, biopsies were taken in the sigmoid colon (n=21), ascending/descending colon (n=25) and the terminal ileum (n=12). In patients with Crohn's disease, biopsies were taken in the ascending/descending colon (n=107) and terminal ileum (n=70) in uninflamed areas in all patients; in patients with mucosal lesions, additional biopsies were taken in inflamed regions of the ascending/descending colon (n=35) and terminal ileum (n=55). In ulcerative colitis patients, paired uninflamed sigmoid (n=48) and inflamed sigmoid biopsies (n=46) were taken. Biopsies were placed in RNAlater at the clinical site, frozen and shipped to Genentech, where they were disrupted using TissueLyzer beads, then RNA was isolated using RNeasy columns. RNA was hybridized to Agilent human 4x44kv1 arrays, dual channel, using universal reference.
2021-07-26 | GSE179285 | GEO
Project description:Microarrays were used to analyze the gene expression in endoscopic-derived intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) and controls Mucosal biopsies were obtained at endoscopy from the colon of 97 ulcerative colitis (UC), 8 Crohn's disease (CD) patients and 11 controls. The biopsies were taken at the most affected sites but at a distance of ulcerations. Disease activity was endoscopically assessed. Total RNA extracted from mucosal biopsies was used to analyze mRNA expression via Affymetrix Human Gene 1.0 ST arrays
2015-05-27 | E-GEOD-59071 | biostudies-arrayexpress
Project description:Analysis of miRNA expression in colon biopsies from Crohn's disease (CD), ulcerative colitis (UC), and non-inflammatory bowel disease (IBD) control subjects.
2014-12-31 | GSE53867 | GEO
Project description:Study 1: Transcriptomic profiles in colon tissue from inflammatory bowel diseases patients in relation to N-nitroso compound exposure and colorectal cancer risk Study 1: N-nitroso compounds (NOC) have been suggested to play a role in human cancer development but definitive evidence is still lacking. In this study we investigated gene expression modifications induced in human colon tissue in relation to NOC exposure to gain insight in the relevance of these compounds in human colorectal cancer (CRC) development. Since there are indications that inflammation stimulates endogenous NOC formation, the study population consisted of patients with inflammatory bowel disease (IBD) and irritable bowel syndrome patients as controls without inflammation. Strong transcriptomic differences were identified in colonic biopsies from IBD patients and compared to controls that enhance the understanding of IBD pathophysiology. However, fecal NOC levels were not increased in IBD patients, suggesting that inflammation did not stimulate NOC formation. By relating gene expression changes of all subjects to fecal NOC levels, we did, however, identify a NOC exposure-associated transcriptomic response that suggests that physiological NOC concentrations may induce genotoxic responses and chromatin modifications in human colon tissue, both of which are linked to carcinogenicity. In a network analysis, chromatin modifications were linked to 11 significantly modulated histone genes, pointing towards a possible epigenetic mechanism that may be relevant in comprehending the molecular basis of NOC-induced carcinogenesis. We conclude that NOC exposure is associated with gene expression modifications in the colon that may increase CRC risk in humans. Study 2: Red meat intake-induced increases in fecal water genotoxicity correlate with pro-carcinogenic gene expression changes in the human colon Study 2: Red meat consumption is associated with an increased colorectal cancer (CRC) risk, which may be due to an increased endogenous formation of genotoxic N-nitroso compounds (NOCs). To assess the impact of red meat intake on potential risk factors of CRC, we investigated the effect of a 7-day dietary red meat intervention in human subjects on endogenous NOC formation and fecal water genotoxicity in relation to transcriptomic changes induced in colonic tissue. In order to evaluate the potential effect of an inflamed colon on endogenous nitrosation, the study population consisted of inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) control subjects without inflammation. The intervention had no effect on fecal NOC formation but fecal water genotoxicity significantly increased in response to red meat intake. Since IBD patients showed no difference in fecal NOC formation or fecal water genotoxicity levels as compared to IBS controls, for transcriptomic analyses, all subjects were grouped together. Genes significantly correlating with the increase in fecal water genotoxicity were involved in biological pathways indicative of genotoxic effects, including modifications in DNA damage, cell cycle, and apoptosis pathways. Moreover, WNT signaling and nucleosome remodeling pathways were modulated that are known to play a part in the carcinogenic process in the human colon. These results are in line with a possible oxidative effect of dietary heme. We conclude that the gene expression changes identified in this study corroborate the genotoxic potential of diets high in red meat and point towards a possible risk of CRC development in humans. The study investigated transcription levels in human colon biopsies obtained during a colonoscopic exam in 32 subjects suffering from either inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS). IBS patients served as control patients for comparison with IBD patients (see Study 1). 12 of these patients (6 IBD and 6 IBS) also followed a 7-day diet high in red meat (300 grams/day) after which a second colonscopic exam was performed to obtain colon biopsies to investigate the effect of the red meat intervention (Study 2). For each subject, cRNA copies of mRNA isolated from the colon biopsies were labeled with one dye (Cy3) and each sample was hybridized on a separate array. One replicate per subject or before/after red meat intervention (so 44 arrays in total, i.e. 20 before patients and 12 before and after patients).
2011-02-01 | E-GEOD-25220 | biostudies-arrayexpress
Project description:Colon gene expression in human IBD. The three major clinical subsets of Inflammatory Bowel Disease (IBD) include colon-only Crohn's Disease (CD), ileo-colonic CD, and Ulcerative Colitis (UC). These experiments tested differential colon gene expression in these three types of IBD, relative to healthy control samples, and the local degree of mucosal inflammation as measured by the CD Histological Index of Severity (CDHIS). Colon biopsy samples were obtained from IBD patients at diagnosis and during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, with a focus upon candidate genes identified in a recent genome wide association study in pediatric onset IBD. Data suggested that two of these candidate genes are up regulated in pediatric IBD, partially influenced by local mucosal inflammation. These experiments tested differential colon gene expression in healthy, CD, and UC samples for candidate genes identified in a recent pediatric onset IBD genome wide association study. Keywords: Single time point in CD and UC and healthy controls. Colon RNA was isolated from biopsies obtained from CD and UC at diagnosis and during therapy 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 1,2,3,4,5) used for normalization of the Sample VALUEs are also contained within this data set.
2009-03-10 | E-GEOD-10616 | biostudies-arrayexpress
Project description:CD326+ sorted intestinal epithelial cells from foetal (9-12 wk gestational age) small bowel and large bowel, CD326+ sorted intestinal epithelial cells from mucosal biopsies of paediatric (5-15 years of age) terminal illeum, ascending colon and sigmoid colon FPG=Foetal proximal gut, FDG=Foetal distal gut, PTI=paediatric terminal ileum, PAC=paedaitric ascending colon, PSC=paediatric sigmoid colon
2015-09-15 | E-MTAB-3704 | biostudies-arrayexpress
Project description:CD326+ sorted intestinal epithelial cells from foetal (9-12 wk gestational age) small bowel and large bowel, CD326+ sorted intestinal epithelial cells from mucosal biopsies of paediatric (5-15 years of age) terminal illeum, ascending colon and sigmoid colon FPG=Foetal proximal gut, FDG=Foetal distal gut, PTI=paediatric terminal ileum, PAC=paedaitric ascending colon, PSC=paediatric sigmoid colon
2015-09-15 | E-MTAB-3703 | biostudies-arrayexpress
Project description:We used microarrays to identify mucosal gene signatures predictive of response to infliximab (IFX) in patients with inflammatory bowel disease (IBD) and to gain more insight into the pathogenesis of IBD. Keywords: drug response and treatment effect Mucosal biopsies were obtained at endoscopy in actively inflamed mucosa from 61 IBD patients (24 ulcerative colitis (UC), 19 Crohnâs colitis (CDc) and 18 Crohnâs ileitis (CDi)), refractory to corticosteroids and/or immunosuppression, before and 4-6 weeks after (except for 1 CDc patient) their first infliximab infusion and in normal mucosa from 12 control patients (6 colon and 6 ileum). The patients were classified for response to infliximab based on endoscopic and histologic findings at 4-6 weeks after first infliximab treatment. Total RNA was isolated from intestinal mucosal biopsies, labelled and hybridized to Affymetrix Human Genome U133 Plus 2.0 Arrays.
2009-11-02 | E-GEOD-16879 | biostudies-arrayexpress
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