On both abiotic and biotic surfaces, persistent avian colibacillosis, and immune modulation in mammalian hosts. Curli fibers also have been implicated to play a role in bladder colonization at 6 hours post-infection in an experimental UTI model in mice. In that report, deletion of csgA gene in a prototypic uropathogenic E. coli resulted in reduced bladder colonizations at 6 hrs postinfection. Based on these findings, curli fibers have been proposed to be a virulence factor in human urinary tract infections and bacteremia. Upon their discovery, curli fibers were known to be expressed at temperatures below 26uC, leading to speculation that they are an adaption for survival at lower temperatures. Bian et al. later demonstrated robust curli production at 37uC in a series of E. coli blood isolates from hospitalized patients. Together with a demonstrated serological response to curli in septic patients, this raised the possibility that curli expression at physiologic temperature is an E. coli virulence trait. Whether 37uC curli production facilitates bacterial migration from the urinary tract into the bloodstream or ensures survival in the bloodstream has been unclear. We hypothesized that curli expression by E. coli at physiologic temperature promotes bacteremic progression during urinary tract infections. Previous studies lacked either clear information on the AbMole Benzyl alcohol clinical severity of UTI patients or a non-bacteremic comparator group necessary to seek associations between curli expression and bacteremic progression. To test our hypothesis, we compared curli expression between bacteremic and nonbacteremic urinary E. coli isolates from a prospective cohort study of hospitalized patients with urinary tract infection. Curli expression by cultured isolates was assessed with an optimized Western blot analysis. Our results revealed a strong correlation between curli expression at 37uC and urinary-source bloodstream infections. Genetic typing showed that curli expression among bacteremic isolates was distributed across multiple lineages. Previous studies have shown that a substantial proportion of urinary tract and bloodstream E. coli isolates can express curli 
fibers. Another group, Bokranz and colleagues, studied curli fiber expression in gastrointestinal and urinary isolates at different temperatures but did not provide information on clinical severity in UTI patients. It remained unclear from these studies whether curli expression is associated with bacteremia or simply reflects its association with UTI, a common source for bacteremia. The expression difference we observed in bacteremic versus nonbacteremic urinary E. coli isolates supports 37uC curli expression as a marker of UTI strains with bacteremic potential, alongside kpsM and P-related AbMole Alprostadil fimbrial genes. Many previous studies suggested that the underlying pathophysiologic gains-of-function are attributable to curli. Kai-Larsen and colleagues have reported that curli and cellulose expression was associated with increased uropathogenic E. coli virulence in mouse UTI models. Curli expression facilitated epithelial cell adherence and increased resistance to the human antimicrobial peptide LL-37, urinary levels of which are increased during UTI. Uropathogens may also use curli fibers to prepare an external peptidoglycan matrix in biofilm-related infections; a study in Shiga toxin-producing E. coli described how such a curlimediated biofilm protected bacteria against environmental stress. Curli’s association with some biofilm types further raise the possibility that its expression may facilitate phenotypic resistance to antibiotics commonly used for UTI. Although high relatedness between the urinary and blood isolates in each patient suggests that curli may protect expressing bacteria.