Uroepithelial bacterial adhesion

Uroepithelial bacterial adhesion is the critical initial step in the pathogenesis of urinary tract infections (UTIs), primarily mediated by uropathogenic Escherichia coli (UPEC) [1]. This process involves the binding of bacterial surface organelles, such as type 1 fimbriae (specifically the FimH adhesin), to mannosylated glycoproteins called uroplakins (e.g., UPK1A) on the surface of the bladder epithelium [2, 3]. By adhering to the host cells, bacteria avoid being flushed out by urine flow and can subsequently invade the tissue or form biofilms [4]. Therapeutic strategies targeting this process, known as anti-adhesive therapy, aim to block these interactions using mannose analogs or specific small-molecule inhibitors like Sibofimloc [5, 6]. This approach is particularly attractive as it exerts less selective pressure for antibiotic resistance compared to traditional bactericidal agents [7]. Sources: [1] Flores-Mireles, A. L., et al. (2015). Nature Reviews Microbiology. [2] Zhou, G., et al. (2001). Journal of Biological Chemistry. [3] Wu, X. R., et al. (1996). Proceedings of the National Academy of Sciences. [4] Spaulding, C. N., et al. (2017). Nature. [5] Kranjčec, B., et al. (2014). BJU International. [6] Sauer, M. M., et al. (2019). Nature Communications. [7] Ofek, I., et al. (2003). FEMS Immunology & Medical Microbiology.

Other names

Bacterial adherence to uroepitheliumUropathogenic E. coli adhesionFimH-mediated adhesionUrothelial bacterial attachmentAnti-adhesive therapy target

Competitive inhibition of bacterial adhesins (e.g., FimH) binding to host urothelial receptors (e.g., Uroplakins).