Interaction of enteropathogenic or enterohemorrhagic Escherichia coli with HeLa cells results in translocation of cortactin to the bacterial adherence site

Infect Immun. 2000 Jan;68(1):382-6. doi: 10.1128/IAI.68.1.382-386.2000.

Abstract

Infection of cultured HeLa epithelial cells with enteropathogenic Escherichia coli (EPEC) or enterohemorrhagic E. coli (EHEC) O157:H7 results in accumulation of cortactin under the adherent bacteria. Tyrosine phosphorylation of cortactin is not induced following HeLa cell infection with EHEC or EPEC, contrary to what has been reported to occur with Shigella flexneri.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Bacterial Adhesion / physiology*
  • Binding Sites
  • Cortactin
  • Cytochalasin D / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Escherichia coli / pathogenicity*
  • Escherichia coli / physiology
  • Escherichia coli O157 / pathogenicity*
  • Escherichia coli O157 / physiology
  • HeLa Cells
  • Humans
  • Microfilament Proteins / physiology*
  • Microscopy, Confocal
  • Phosphorylation
  • Protein Binding
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Shigella flexneri / pathogenicity
  • Shigella flexneri / physiology
  • Staurosporine / pharmacology
  • Tyrosine / metabolism
  • Virulence

Substances

  • Actins
  • CTTN protein, human
  • Cortactin
  • Enzyme Inhibitors
  • Microfilament Proteins
  • Cytochalasin D
  • Tyrosine
  • Protein-Tyrosine Kinases
  • Staurosporine