ArticleJCI insight2024
MUC17 is an essential small intestinal glycocalyx component that is disrupted in Crohn's disease.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- MUC17 and the intestinal glycocalyx: structure, regulation, and barrier function in health and disease.Bioscience reports · 2026Review
- Developmental factors drive the compartmentalized and discontinuous maturation of the small intestinal epithelium during the early postnatal period.PLoS biology · 2026Article
- B3GNT7 regulates mucin glycosylation and protects against colitis and infection.bioRxiv : the preprint server for biology · 2026Article
- The HUNT study identifies host genetic factors reproducibly associated with human gut microbiota composition.Nature genetics · 2026Article
- Spatial transcriptomic analysis of foveolar-type gastric adenoma with raspberry-like appearance.Virchows Archiv : an international journal of pathology · 2026Article
- Short Ileal Microvillus Length Phenotype Associates with Progression from Inflammatory to Complicated Disease Behavior in Pediatric Crohn's Disease.Inflammatory bowel diseases · 2026Article
- Defining enteric bacterial pathogenesis using organoids:Gut microbes · 2025Article
- Unravelling key genes and molecular pathways in gastric inflammation-to-cancer transition through causal discovery: implications for early diagnosis and therapy.SAGE open medicine · 2025Article
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Abstract
Crohn's disease (CD) is the chronic inflammation of the terminal ileum and colon triggered by a dysregulated immune response to bacteria, but insights into specific molecular perturbations at the critical bacteria-epithelium interface are limited. Here, we report that the membrane mucin MUC17 protected small intestinal enterocytes against commensal and pathogenic bacteria. In noninflamed CD ileum, reduced MUC17 levels and a compromised glycocalyx barrier allowed recurrent bacterial contact with enterocytes. Muc17 deletion in mice rendered the small intestine particularly prone to atypical bacterial infection while maintaining resistance to colitis. The loss of Muc17 resulted in spontaneous deterioration of epithelial homeostasis and in the extraintestinal translocation of bacteria. Finally, Muc17-deficient mice harbored specific small intestinal bacterial taxa observed in patients with CD. Our findings highlight MUC17 as an essential region-specific line of defense in the small intestine with relevance for early epithelial defects in CD.
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