Dr fimbriae operon of uropathogenic Escherichia coli mediate microtubule-dependent invasion to the HeLa epithelial cell line

J Infect Dis. 1997 Jul;176(1):158-67. doi: 10.1086/514018.


Escherichia coli Dr adhesin and decay-accelerating factor (DAF) receptor-mediated interaction was proposed as the mechanism of ascending urinary tract infection (UTI) and chronic interstitial nephritis. This report provides novel evidence for Dr fimbriae operon-mediated invasive capacity of Dr+ E. coli. Insertional mutants draE, draC, and draB, and adherent draD and UV-inactivated BN406 were unable to enter HeLa cells. Complementation of the dra mutation restored invasiveness. Internalization was inhibited by anti-Dr fimbriae IgG (100%), anti-SCR-3 domain of DAF (75%), and nocodazole (95%). Increased receptor-ligand density occurred at the site of internalization. Internalized Dr+ E. coli did not significantly multiply in the HeLa cell line. Accordingly, the dra operon and DAF were required for microtubule-dependent internalization of E. coli to HeLa cells. The relatively low invasion and multiplication rates of Dr+ E. coli may hypothetically contribute to the postattachment steps of ascending UTI and chronic renal infection.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adhesins, Escherichia coli / analysis
  • Adhesins, Escherichia coli / genetics*
  • Bacterial Adhesion
  • CD55 Antigens / analysis
  • CD55 Antigens / physiology
  • Cytochalasin D / pharmacology
  • Escherichia coli / genetics
  • Escherichia coli / pathogenicity*
  • HeLa Cells
  • Humans
  • Immunohistochemistry
  • Microscopy, Electron
  • Microtubules / physiology*
  • Nocodazole / pharmacology
  • Operon*
  • Urinary Tract Infections / microbiology*


  • Adhesins, Escherichia coli
  • CD55 Antigens
  • Cytochalasin D
  • Nocodazole