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Bacterial adhesion to intestinal and urinary tract mucosa is a complex biological process that serves as the initial step in the pathogenesis of various infections. This process involves the specific interaction between bacterial surface proteins, known as adhesins such as FimH on type 1 fimbriae, and host cell receptors including uroplakins in the bladder or CEACAM6 in the intestinal epithelium (Sauer et al., 2019, Nature Reviews Microbiology). By adhering to these surfaces, bacteria like uropathogenic Escherichia coli (UPEC) and adherent-invasive E. coli (AIEC) can resist mechanical clearance by urine flow or intestinal peristalsis, allowing for colonization and biofilm formation (Spaulding et al., 2017, Nature). This mechanism is a key driver in diseases such as recurrent urinary tract infections and Crohn's disease (Barnich et al., 2007, J. Clin. Invest.). Therapeutic interventions, often referred to as anti-adhesion therapies, utilize small molecules like D-mannose or targeted inhibitors like sibofimloc to competitively block these binding sites. This approach aims to prevent or treat infections without exerting the same selective pressure as traditional antibiotics, potentially reducing the development of antimicrobial resistance (Mydock-McGrane et al., 2016, Expert Opin. Ther. Pat.). Furthermore, targeting these interactions provides a localized treatment strategy that can minimize systemic side effects. Research continues to explore the efficacy of these agents in both acute and chronic inflammatory conditions where bacterial persistence is a factor.
Competitive inhibition of bacterial adhesins binding to host cell surface receptors.
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