FIMBRIAE AND FLAGELLA MEDIATED SURFACE MOTILITY AND THE EFFECT OF GLUCOSE ON NONPATHOGENIC AND UROPATHOGENIC ESCHERICHIA COLI

ABSTRACT We characterized the surface motility of nonpathogenic and pathogenic E. coli strains with respect to the appendage requirement, flagella versus fimbriae, and the glucose requirement. Nonpathogenic lab strains exhibited either slow or fast surface movement. The slow strains required type 1 fimbriae for movement, while the fast strains required flagella and had an insertion in the flhDC promoter region. Surface movement of three uropathogenic E. coli (UPEC) strains was fast and required flagella, but these strains did not have an insertion in the flhDC promoter region. We assessed swimming motility as an indicator of flagella synthesis and found that glucose inhibited swimming of the slow nonpathogenic strains but not of the fast nonpathogenic or pathogenic strains. Fimbriae-based surface motility requires glucose, which inhibits cyclic-AMP (cAMP) and flagella synthesis; therefore, we examined whether surface motility required cAMP. The surface motility of a slow, fimbriae-dominant, nonpathogenic strain did not require cAMP, which was expected because fimbriae synthesis does not require cAMP. In contrast, the surface motility of a faster, flagella-dominant, UPEC strain required cAMP, which was unexpected because swarming was unaffected by the presence of glucose. Electron microscopy verified the presence or absence of fimbriae or flagella. In summary, surface motilities of the nonpathogenic and uropathogenic E. coli strains of this study differed in the appendage used and the effects of glucose on flagella synthesis. IMPORTANCE Uropathogenic Escherichia coli strains cause 80-90% of community-acquired urinary tract infections, and recurrent urinary tract infections, which can last for years, and often become antibiotic resistant. Urinary tract infections can be associated with intra-vesical lesions extending from localized trigonitis/cystitis to widely distributed pancystitis: motility may be a factor that distinguishes between these infection patterns. Nonpathogenic and uropathogenic E. coli were shown to exhibit fimbriae- and flagella-dependent surface motility, respectively, and the difference was attributed to altered control of flagella synthesis by glucose. Uropathogenic E. coli strains grow more rapidly in urine than nonpathogenic strains, which implies differences in metabolism. Understanding the basis for glucose-insensitive control of flagella-dependent motility could provide insight into uropathogenic E. coli metabolism and virulence.