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The attachment of uropathogenic bacteria, especially *Escherichia coli*, to the urothelium is a key event in the development of urinary tract infections. This adhesion is primarily mediated by bacterial type 1 fimbriae and their adhesin FimH, which bind specifically to the uroplakin receptor complex (notably UPIa) on the surface of urothelial cells[1][6]. This molecular interaction triggers host cell signaling, facilitates bacterial invasion, and may lead to intracellular bacterial communities, biofilm formation, and recurrent infections. Targeting this adhesion step is a promising strategy for UTI prevention and treatment—for example, by blocking FimH binding, interfering with receptor glycosylation, or using agents like D-mannose or dictamnine that disrupt the bacterial–host interface[5][6].
Competitive inhibition of FimH–uroplakin interaction (e.g., D-mannose mimics the uroplakin glycoprotein binding site to block FimH-mediated adhesion); Inhibition of bacterial fimbriae expression or function; Modulation of host receptor density or glycosylation
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