Uropathogenic Escherichia coli fimbriae and related surface adhesion structures (UPEC adhesins)

Uropathogenic Escherichia coli (UPEC) fimbriae and related surface adhesion structures are critical virulence factors that mediate the attachment of bacteria to the host urinary tract epithelium. The most prominent structures include Type 1 fimbriae, which utilize the FimH adhesin to bind mannosylated uroplakins in the bladder, and P fimbriae, which employ PapG to target galabiose-containing glycolipids in the kidneys (Sivick & Mobley, 2010). These structures are assembled via the chaperone-usher pathway and are essential for colonization, biofilm formation, and invasion into host cells, allowing UPEC to persist against the flow of urine and host immune responses (Waksman & Hultgren, 2009). Targeting these adhesins, particularly FimH, represents a promising non-antibiotic therapeutic strategy to prevent and treat urinary tract infections (UTIs) by blocking the initial stages of infection (Spaulding et al., 2017). Current pharmacological approaches include mannoside-based competitive inhibitors, pilicides that disrupt pilus biogenesis, and vaccine candidates targeting fimbrial subunits (Greene et al., 2015).

Other names

UPEC piliType 1 fimbriaeP fimbriaeFimH adhesinPapG adhesinDr adhesinsS fimbriaeCurli fibersAfa/Dr adhesinsChaperone-usher pili

The primary mechanism of action involves the competitive inhibition of bacterial adhesins, such as FimH, preventing their binding to mannosylated host receptors (Sivick & Mobley, 2010). Additionally, small molecule pilicides can disrupt the chaperone-usher pathway, preventing the assembly of functional fimbriae on the bacterial surface (Waksman & Hultgren, 2009).