Animal model of Crohn’s disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB10309 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR982849.fastq.gz | Fastqsanger.gz | |||
| ERR982850.fastq.gz | Fastqsanger.gz | |||
| ERR982851.fastq.gz | Fastqsanger.gz | |||
| ERR982852.fastq.gz | Fastqsanger.gz | |||
| ERR982853.fastq.gz | Fastqsanger.gz |
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Project description:Experimental colitis is often used as a model for the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease. Results identify the inflammatory processes during acute colitis in affected tissues from TNBS-treated susceptible 5-7 week old SJL mice. Keywords: Disease state analysis
2008-09-08 | GSE12139 | GEO
Project description:Experimental colitis is often used as a model for the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease. Results identify the inflammatory processes during acute colitis in affected tissues from TNBS-treated susceptible 5-7 week old SJL mice. Keywords: Disease state analysis Two-condition experiment, Treated vs Non-treated. Biological replicates: 4 treated, 4 non-treated. One replicate per array.
2008-09-08 | E-GEOD-12139 | biostudies-arrayexpress
Project description:<p><strong>INTRODUCTION:</strong> Crohn’s disease (CD) is a chronic, relapsing inflammatory bowel disease affecting the gastrointestinal tract. Although its precise etiology has not been fully elucidated, imbalance of the intestinal microbiota has been known to play a role in CD. Fecal metabolites may be related to the onset and progression of CD.</p><p><strong>OBJECTIVES:</strong> This study aimed to clarify the transition of fecal metabolites associated with disease progression using SAMP1/YitFc mice, mouse models of spontaneous CD.</p><p><strong>METHODS:</strong> Feces from control ICR (n = 6) and SAMP1/YitFc (n = 8) mice at different ages were subjected to 1H nuclear magnetic resonance (NMR) analysis. The obtained NMR spectra were used for multivariate and quantitative analyses.</p><p><strong>RESULTS:</strong> Fecal metabolites, such as short-chain fatty acids, lactate, glucose, xylose, and choline, dramatically fluctuated with disease progression before histological abnormalities associated with CD were apparent in SAMP1/YitFc mice. Unlike that of other metabolites, fecal taurine concentration in SAMP1/YitFc was high regardless of age.</p><p><strong>CONCLUSION:</strong> The fecal metabolites showing characteristic fluctuations may be utilized as potential biomarkers in predicting CD pathology.</p>
2020-02-09 | MTBLS1209 | MetaboLights
Project description:Fibrostenotic disease is a common complication in Crohn’s disease (CD). We performed bulk RNA sequencing (n=16) of paired intestinal biopsies taken from nonstenotic and stenotic areas of patients with CD (n=8).
2023-04-26 | E-MTAB-12788 | biostudies-arrayexpress
Project description:Intestinal microbial dysbiosis is associated with Crohn’s disease (CD). However, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease remain unclear. To evaluate causality and mechanisms of disease, we conducted a systems level study of the interactions between the gut microbiota and host in new-onset pediatric patients. We report an altered host proteome in CD patients indicative of impaired mitochondrial functions. A downregulation of mitochondrial proteins implicated in H2S detoxification was observed, while the relative abundance of H2S microbial producers was increased. Network correlation analysis identified Atopobium parvulum as the central hub of H2S producers. Gnotobiotic and conventionalized colitis-susceptible interleukin-10-deficient (Il10-/-) mice demonstrated that A. parvulum induced colitis, a phenotype requiring the presence of the intestinal microbiota. Administration of bismuth, a H2S scavenger, prevented A. parvulum-induced colitis in Il10-/- mice. This study identified host-microbiota interactions that are disturbed in CD patients providing mechanistic insights on CD pathogenesis.
2016-09-29 | PXD002882 | Pride
Project description:To investigate the mechanism of demethylase FTO in Crohn's disease，We used m6A MeRIP-seq data from three normal colon samples and three TNBS-induced IBD colon samples of C57 mice for gene expression profiling.
2024-11-09 | GSE280813 | GEO
Project description:Objective Crohn’s Disease (CD) and Ulcerative Colitis (UC) are chronic inflammatory diseases of the gastrointestinal tract. Reliable diagnosis of these diseases requires a comprehensive examination of the patient, which include invasive endoscopy. This study assesses whether non-invasive LC-MS/MS based analysis of microbial and human proteins from feces may support the diagnosis of the diseases. Design In order to mimic a representative clinical background for this study, we investigated 17 healthy controls, 11 CD patients, 14 UC patients, also 13 Irritable Bowel Disease (IBS) patients, 8 Colon Adenoma (CA) patients, and 8 Gastric Carcinoma (GCA) patients. The proteins were extracted from the fecal samples with liquid phenol in a ball mill. Subsequently, the proteins were digested tryptically to peptides and analyzed by liquid chromatography coupled to an Orbitrap MS/MS. For protein identification and interpretation of taxonomic and functional results, the MetaProteomeAnalyzer software and the UniProtKB/SwissProt database and several metagenomes from human fecal samples were used. Results Cluster analysis and ANOSIM show a separation of healthy controls from patients with CD and UC as well as from patients with GCA. Among others, UC and CD correlated with an increase of neutrophil extracellular traps and immunoglobulins G (IgG) as well as a decrease of IgA. A specific marker metaprotein for CD was an increase of the human enzyme sucrose-isomaltase. IBS and CA patient’s fecal metaproteome showed only minor alterations. Conclusion Metaproteome analysis distinguished between patients with UC, CD and healthy controls and is therefore useful as a non-invasive tool for routine diagnostics in hospitals.
2019-03-11 | PXD010371 | Pride
Project description:Crohn’s disease is a relapsing inflammatory disorder with a variable clinical course. While most patients present with purely an inflammatory phenotype (B1) at diagnosis, a subgroup (~20%) rapidly progresses to complicated disease manifestations that include stricturing (B2) within 5 years. DNA methylation is a key epigenetic mechanism that can regulate gene expression and thereby influence the development and progression of complex diseases. Site-specific DNA methylation differences have been reported in peripheral blood of patients with Crohn’s disease, but investigation of the temporal relationship between methylation and disease is required to establish whether the methylome plays a causal role and can be leveraged for therapeutic benefits. To this end, we conducted an epigenome-wide study of methylation (~850K sites) in peripheral blood at diagnosis and during follow-up from the RISK pediatric Crohn’s disease inception cohort. While some methylation changes associated with Crohn’s disease might be causal, in peripheral blood the vast majority are found to be a transient consequence of inflammation and thus a symptom of disease.
2018-04-03 | GSE112611 | GEO
Project description:The interpretation of transcriptional profiling studies of intestinal tissue from Crohn’s disease patients and control patients can be confounded by differing proportions of cell subsets (e.g. immune cells) present in these samples. In this study, we aimed to control for cellular composition using standard, archival formalin-fixed, paraffin-embedded (FFPE) tissue specimens from Crohn’s patients (n=36) and controls (n=32) who underwent intestinal resection surgery. This approach allowed us to use the same tissue specimens for histological screening to select study samples with similar cellular composition and for RNA extraction for RNA-seq transcriptional profiling. We hypothesized that this approach would allow us to more clearly identify molecular signatures in ileal tissue that were associated with Crohn’s disease-associated pathological mechanisms.
2018-05-22 | E-MTAB-5790 | biostudies-arrayexpress
Project description:Crohn’s disease is characterized by transmural inflammation and therefore the mesenteric immune compartment has gained interest. However, its significance in Crohn’s disease is largely unclear. Macrophages are plastic cells that adapt their phenotype to environmental stimuli resulting in inflammatory and regulatory macrophage subsets. Hence, their distribution can reflect the overall nature of an immune infiltrate. We show that mesenteric macrophages contain two populations, characterized as CD11b-high and CD11b-dim. The CD11b-dim population is characterized by expression of regulatory markers CD206, CD200R, CD163, PD-L2, CD32. CD11b-high macrophages display an IFNγ induced signature and produce high levels of calprotectin. CD11b-dim and CD11b-high populations were comparable between Crohn’s disease and other indications in expression pattern, but the CD11b-high population was strongly overrepresented in this patient group.
2021-04-07 | GSE148233 | GEO