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Intestinal epithelial cell surface mannose residues are carbohydrate structures, specifically terminal mannose sugars, found on the glycoproteins and glycolipids of the intestinal mucosa [1]. These residues play a pivotal role in the gut's ecosystem by serving as attachment points for both beneficial and pathogenic bacteria, such as Type 1 fimbriated Escherichia coli [2]. In certain pathological conditions like Crohn's disease, the expression of mannosylated proteins such as CEACAM6 is significantly upregulated, providing an expanded niche for Adherent-Invasive E. coli (AIEC) to colonize and trigger inflammatory cascades [3][4]. Therapeutic interventions targeting this interaction often utilize mannose mimetics or decoys, such as D-mannose or small-molecule FimH antagonists like Sibofimloc, which competitively bind to bacterial lectins to prevent their attachment to the intestinal wall [5][6]. By blocking this initial step of colonization, these agents aim to reduce the bacterial burden and associated mucosal inflammation without the use of traditional antibiotics [7].
Competitive inhibition of bacterial lectin (e.g., FimH) binding to host mannose residues
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