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Intestinal mucosal pathogen binding sites are a diverse collection of host-derived molecules, including glycoproteins, glycolipids, and mucins, that facilitate the attachment and colonization of the gastrointestinal tract by various pathogens (Ribet & Cossart, 2015). These sites, such as mannose-containing glycans and sialic acid residues, are recognized by specific microbial adhesins, allowing pathogens to resist mechanical clearance and initiate infection (Sharon, 2006). Common host receptors involved include members of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family and various histo-blood group antigens (Moonens & Remaut, 2014). Therapeutic strategies targeting these sites often employ anti-adhesion agents, such as carbohydrate decoys or competitive probiotics, which mimic host receptors to intercept pathogens before they can bind to the epithelium (Bode, 2012). For example, human milk oligosaccharides act as natural decoys that protect infants from enteric infections by saturating pathogen binding sites (Bode, 2012). By preventing the initial step of infection, these therapies offer a non-antibiotic approach to managing enteric diseases, potentially reducing the risk of antimicrobial resistance (Ofek et al., 2003).
Competitive inhibition of pathogen attachment to host mucosal receptors, thereby preventing colonization and subsequent infection (Ofek et al., 2003).
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