Abstract

Bacterial attachment is thought to enhance virulence by promoting colonization of the urinary tract and by attacking tissue [1]. Uropathogenic Escherichia coli express several classes of fimbriae-associated adhesins that mediate attachment through specific binding to different glycoconjugate receptors [2] (for review see Mirelman [3]). P fimbriae, encoded by the pap gene cluster, show the most clear-cut association with virulence as defined by acute disease severity [4]. It has been proposed that P fimbriae augment the virulence of uropathogenic E. coli at different stages during the pathogenesis of urinary tract infection (UTI). pap+ strains remain longer in the intestinal flora and spread more efficiently to the urinary tract than do papstrains [5]. Once in the urinary tract, P-fimbriated strains establish bacteriuria and may cross the epithelial barrier into the bloodstream [6]. P fimbriae enhance epithelial cytokine responses in vitro [7] and in the mouse UTI model [8]. The role of P fimbriae per se for colonization and host response induction is not clear and has been the subject of some discussion. While fimbriae-mediated attachment enhances bac-

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