Intestinal enterocyte mannose residues

Intestinal enterocyte mannose residues are carbohydrate structures located on the apical surface of the intestinal epithelium, primarily as part of N-linked glycans on glycoproteins such as Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) [1][2]. These residues serve as critical docking sites for various Gram-negative pathogens, most notably Adherent-Invasive Escherichia coli (AIEC) and uropathogenic E. coli (UPEC), which express the mannose-binding adhesin FimH on their type 1 fimbriae [2][3]. The interaction between bacterial FimH and these host mannose residues facilitates bacterial colonization, biofilm formation, and subsequent invasion of the intestinal mucosa, a process heavily implicated in the pathogenesis of Crohn's disease and the maintenance of a gut reservoir for recurrent urinary tract infections [3][4]. Therapeutic strategies targeting these residues involve the administration of exogenous D-mannose or high-affinity small-molecule FimH antagonists like Sibofimloc, which act as molecular decoys [5]. By competitively binding to the bacterial FimH protein, these agents prevent the pathogens from adhering to the intestinal wall, thereby promoting their clearance from the gastrointestinal tract and reducing inflammation [1][5]. This anti-adhesive approach represents a significant non-antibiotic alternative for managing chronic inflammatory conditions and preventing infectious diseases without contributing to antimicrobial resistance [4][5]. Sources: [1] Bouckaert, J., et al. (2005). Molecular Microbiology. [2] Barnich, N., et al. (2007). Journal of Clinical Investigation. [3] Wellens, A., et al. (2008). Expert Review of Anti-infective Therapy. [4] Kranjčec, B., et al. (2014). World Journal of Urology. [5] Sivignon, A., et al. (2015). Expert Opinion on Investigational Drugs.

Other names

Mannosylated glycoproteinsD-mannose moietiesHost cell mannose residuesType 1 fimbriae receptorsN-linked mannose glycans

Competitive inhibition of bacterial FimH adhesin binding to host mannosylated receptors, preventing pathogen colonization and mucosal invasion.