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Intestinal epithelial cell surface glycans and mucosal carbohydrates constitute the complex glycocalyx and mucus layers that line the gastrointestinal tract, serving as the primary interface between the host and the external environment [1]. These molecules, which include glycoproteins like mucins and various glycolipids, provide critical binding sites for both beneficial commensal bacteria and harmful pathogens [2]. In healthy individuals, these glycans maintain the structural integrity of the mucosal barrier and regulate the immune system's tolerance to the microbiota [3]. However, alterations in glycan composition are frequently observed in diseases such as inflammatory bowel disease (IBD) and enteric infections, where they can facilitate pathogen attachment or trigger inflammatory cascades [4]. Therapeutically, these carbohydrates are targeted using anti-adhesion strategies, such as small molecule inhibitors like Siboflanstat that prevent bacteria from binding to mannosylated glycans, or decoy molecules like human milk oligosaccharides (HMOs) that mimic host receptors [5]. Understanding the specific glycan signatures is essential for developing targeted therapies for infectious, inflammatory, and neoplastic gastrointestinal disorders [1, 6]. Sources: [1] Nature Reviews Gastroenterology & Hepatology, "The role of glycans in the intestinal barrier." [2] Frontiers in Immunology, "Targeting host-pathogen interactions through glycobiology." [3] Glycobiology, "Human milk oligosaccharides: Every baby needs a sugar mama." [4] Journal of Crohn's and Colitis, "Glycosylation changes in inflammatory bowel disease." [5] ClinicalTrials.gov, "Siboflanstat (EB8018) for the treatment of Crohn's disease." [6] PubMed, "Intestinal glycans as determinants of microbiota composition."
Competitive inhibition of pathogen binding, Decoy receptor activity, Modulation of gut microbiota composition, Enhancement of mucosal barrier function, Inhibition of bacterial adhesion to mannosylated receptors
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