Project description:The IBD-Character cohort (Edinburgh, Oslo, Örebro, Linköping, Zaragoza, Maastricht) included patients with inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) recruited at diagnosis and non-IBD controls. Paired-end RNA sequencing was used for whole blood expression profiling. Raw and normalized counts tables are provided.
Project description:Differences in CD8+ T-cell expression have previously been reported to correlate with disease outcome in adult patients diagnosed with Inflammatory Bowel Diseases (IBD). In addition, T-cell exhaustion was found to be associated with a milder disease course in adults. The purpose of this study was to test the prognostic value of the reported adult T-cell expression and exhaustion signatures in a cohort of children newly diagnosed with Crohn's disease (CD) and ulcerative colitis (UC). We also investigated the possibility of a paediatric specific prognostic expression signature.
Project description:Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is associated with a loss or an imbalance of host-microbe interactions. Depletion-assisted deep metaproteomics was employed to reveal disease-specific networks of host-microbial protein associations in IBD.
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.
Project description:RNA was isolated from rectal biopsies from 190 pediatric patients undergoing diagnostic colonoscopy for inflammatory bowel diseases, including Crohn's disease and ulcerative colitis. Single-end, 75-bp sequencing was performed, and raw reads aligned to the human genome using Gencode v 24 as reference. We included 14085 protein-coding mRNA genes in downstream analyses, where cutoffs of fold change>1.5 and FDR<0.05 were considered significant.
Project description:Primary objectives: To assess the impact of antiTNF agents on the male inflammatory bowel diseases patients` fertility
Primary outcomes:- semen quality and quantity, inclusive sperm chromatine structure analysis prior and during anti-TNF therapy- time to conception
Project description:The series was designed to identify new genes involved in the pathophysiology of inflammatory bowel disease (Crohn's disease and ulcerative colitis). This series represents a group of 31 samples, subdivided into 3 groups: 1) Normal controls: 11 samples; 2) patients with Crohn's diseases: 10 samples; 3) patients with ulcerative colitis: 10 samples. Each sample originated from a different patient or normal control, in total n=31 individuals were examined. Keywords = Inflammatory bowel disease Keywords = Crohn's disease Keywords = ulcerative colitis Keywords = expression screening Keywords = expression profiling Keywords: other
Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.
Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.
Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.