Introduction Uropathogenic E. coli (UPEC) account for the majority of urinary tract infections (UTI). Despite antibiotic treatment, recurrence of infection is frequently reported. Invasion of superficial bladder cells by UPEC and subsequent development of intracellular bacterial communities (IBCs) is one reason of recurrent UTI. Intracellular UPEC are protected from the host immune system and are more resistant to antimicrobial agents. Reservoir formation and subsequent reactivation and exit of UPEC from infected cells contribute to recurrent UTI.

Goals Our aim is to identify (1) if there are any stimuli which trigger bacterial exit from the cells and (2) which bacterial factors are involved in the intracellular life cycle of UPEC especially during the exit from infected cells.

Materials & Methods We use an in vitro bladder epithelial model employing RT-112 bladder epithelial cells. After infection of RT-112 cells with UPEC, the invasion, intracellular survival and the escape of the bacteria from the cells were quantified. The formation of IBCs and the localization of bacteria inside the cells was monitored by fluorescence microscopy.

Results We studied the influence of different glucose concentrations on the development of IBCs. We infected bladder epithelial cells with two different UPEC model isolates. Our results show that these UPEC strains respond differently to varying glucose concentrations in in vitro infection studies. Different glucose concentrations do not only impact the intracellular replication, but also the exit from the host cells by UPEC differentially. Treatment of the cells with either inhibitors of glycolysis or inhibitors of glucose transporters complements the effects seen with different glucose concentrations.

Discussion Our results show that the intracellular life cycle of UPEC is affected by the availability of the carbon source glucose. Interestingly, the two model UPEC strains also differ in growth behavior with glucose as sole carbon source, but show similar multiplication rates in more complex growth media. The mechanism and consequences how glucose affects the UPEC intracellular life cycle and exit remains to be elucidated.