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Gut microbiota and pathogenic bacteria adhesion sites are the molecular interfaces on the intestinal surface where microbes attach to the host. These sites consist of a variety of host-derived components, including transmembrane proteins like Carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) and integrins, as well as the complex carbohydrate structures of the mucus layer, such as those found on MUC2 mucins [1][2]. The binding of bacterial surface structures, termed adhesins (such as fimbriae, pili, or flagella), to these specific host receptors is essential for the establishment of the gut microbiome and the initiation of infection by enteric pathogens [3]. In the context of disease, pathogenic bacteria utilize these adhesion sites to colonize the gut, evade mechanical clearance, and facilitate the delivery of virulence factors into host cells, often leading to inflammation and tissue damage [4]. Therapeutic targeting of these sites involves the use of anti-adhesion agents, such as mannosides or decoy glycans, which competitively inhibit the interaction between bacterial adhesins and host receptors [5]. This approach is particularly valuable as it provides a means to prevent or treat infections and manage inflammatory bowel diseases without the broad-spectrum ecological disruption or resistance pressure associated with traditional antibiotics [6].
Competitive inhibition of bacterial adhesin binding to host cell surface receptors or mucus-associated glycans, preventing microbial colonization and subsequent pathogenesis [5].
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