BACKGROUND: Most uropathogenic Escherichia coli (UPEC) strains harbor genes encoding adhesive type 1 fimbria (T1F). T1F is a key factor for successful establishment of urinary tract infection. However, UPEC strains typically do not express T1F in the bladder urine, and little is understood about its induction in vivo. METHODS: A flow chamber infection model was used to grow UPEC under conditions simulating distinct infection niches in the bladder. Type 1 fimbriation on isolated UPEC was subsequently determined by yeast cell agglutination and immunofluorescence microscopy, and the results were correlated with the ability to adhere to and invade cultured human bladder cells. RESULTS: Although inactive during planktonic growth in urine, T1F expression occurs when UPEC settles on and infects bladder epithelial cells or colonizes catheters. As a result, UPEC in these sessile populations enhances bladder cell adhesion and invasion potential. Only T1F-negative UPEC are subsequently released to the urine, thus limiting T1F expression to surface-associated UPEC alone. CONCLUSIONS: Our results demonstrate that T1F expression is strictly regulated under physiological growth conditions with increased expression during surface growth adaptation and infection of uroepithelial cells. This leads to separation of UPEC into low-expression planktonic populations and high-expression sessile populations.
BACKGROUND: Most uropathogenic Escherichia coli (UPEC) strains harbor genes encoding adhesive type 1 fimbria (T1F). T1F is a key factor for successful establishment of urinary tract infection. However, UPEC strains typically do not express T1F in the bladder urine, and little is understood about its induction in vivo. METHODS: A flow chamber infection model was used to grow UPEC under conditions simulating distinct infection niches in the bladder. Type 1 fimbriation on isolated UPEC was subsequently determined by yeast cell agglutination and immunofluorescence microscopy, and the results were correlated with the ability to adhere to and invade cultured human bladder cells. RESULTS: Although inactive during planktonic growth in urine, T1F expression occurs when UPEC settles on and infects bladder epithelial cells or colonizes catheters. As a result, UPEC in these sessile populations enhances bladder cell adhesion and invasion potential. Only T1F-negative UPEC are subsequently released to the urine, thus limiting T1F expression to surface-associated UPEC alone. CONCLUSIONS: Our results demonstrate that T1F expression is strictly regulated under physiological growth conditions with increased expression during surface growth adaptation and infection of uroepithelial cells. This leads to separation of UPEC into low-expression planktonic populations and high-expression sessile populations.
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