Abstract
The urinary tract environment provides many conditions that deter colonization by microorganisms. D-serine is thought to be one of these stressors and is present at high concentrations in urine. D-serine interferes with L-serine and pantothenate metabolism and is bacteriostatic to many species. Uropathogenic Escherichia coli commonly possess the dsdCXA genetic locus, which allows them to use D-serine as a sole carbon, nitrogen, and energy source. It was previously reported that in the model UPEC strain CFT073, a dsdA mutant outcompetes wild type in the murine model of urinary tract infection. This “hypercolonization” was used to propose a model whereby UPEC strains sense D-serine in the urinary tract and subsequently up-regulate genes necessary for pathogenesis. Here, we show that inactivation of dsdA does not lead to hypercolonization. We suggest that this previously observed effect is due to an unrecognized secondary mutation in rpoS and that some D-serine specific effects described in other studies may be affected by the rpoS status of the strains used. Inactivation of dsdA in the original clinical isolate of CFT073 gives CFT073 ΔdsdA a growth defect in human urine and renders it unable to grow on minimal medium containing D-serine as the sole carbon source. However, CFT073 ΔdsdA is able to colonize the urinary tracts of CBA/J mice indistinguishably from wild type. These findings indicate that D-serine catabolism, though it may play role(s) during urinary tract infection, does not affect the ability of uropathogenic E. coli to colonize the murine urinary tract.
Highlights
Urinary tract infections (UTIs) represent a major public health concern, as they are among the most common human bacterial infections
We previously reported the genome sequence of Uropathogenic Escherichia coli (UPEC) strain CFT073 [40], which was isolated from the blood of a pyelonephritis patient in the late 1980s [41]
Because CFT073 gyrAS83L colonizes mice indistinguishably from its nalS parent [42], CFT073 gyrAS83L strain was previously used as wild type to facilitate enumeration of wild type/mutant ratios during competitive murine model UTI [28, 43]
Summary
Urinary tract infections (UTIs) represent a major public health concern, as they are among the most common human bacterial infections. Uropathogenic Escherichia coli (UPEC) is the most common causative agent of UTIs, representing up to 95% of reported community-acquired cases [3]. UPEC are members of the gut microbiota and gain access to the urinary tract via an ascending route [4]. During this ascent, the bacteria first colonize the periurethral area and traverse the urethra into the bladder, where they cause cystitis. Cystitis can progress to pyelonephritis after the bacteria ascend the ureters into the kidneys of the infected individual
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