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Molecular Profiling of the Appendix in Pediatric Inflammatory Bowel Diseases

ABSTRACT: Clinical studies suggest a critical role for the appendix in the pathogenesis of inflammatory bowel diseases (IBD), including Crohn disease (CD) and ulcerative colitis (UC), as indicated by the presence of peri-appendicular patches in UC and the beneficial effects of appendectomy in UC. However, the underlying mechanisms remain unclear. To address this gap, we characterized microbial species, associated patterns, and host-microbiota interactions in the appendix and non-inflamed regions of the colon tissue and mucus from pediatric IBD and non-IBD patients (n=15). Metagenomic analyses revealed an enrichment of Proteobacteria (p-value=0.0061) and reduced bacterial diversity in IBD patients’ appendix compared to controls. Strong correlations between host tissue and mucus microbial pathways of IBD patients highlighted a link between microbial communities and host gene expression, contributing to immune activation and inflammation in the appendix. Our findings thus provide valuable insights and a basis for mechanistic hypotheses regarding the appendix’s role in IBD pathogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE281635 | GEO | 2026/07/14

REPOSITORIES: GEO

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Appendix metagenome

Project description:Appendix Metagenome

| PRJNA596776 | ENA

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2010-05-27 | E-GEOD-9686 | biostudies-arrayexpress

Human colon expression in healthy, CD, treated CD, and UC

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. Keywords: Single time point in CD, UC, and healthy controls.

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