Invasive and adherent bacterial pathogens co-Opt host clathrin for infection

Cell Host Microbe. 2007 Nov 15;2(5):340-51. doi: 10.1016/j.chom.2007.10.001.


Infection by the bacterium Listeria monocytogenes depends on host cell clathrin. To determine whether this requirement is widespread, we analyzed infection models using diverse bacteria. We demonstrated that bacteria that enter cells following binding to cellular receptors (termed "zippering" bacteria) invade in a clathrin-dependent manner. In contrast, bacteria that inject effector proteins into host cells in order to gain entry (termed "triggering" bacteria) invade in a clathrin-independent manner. Strikingly, enteropathogenic Escherichia coli (EPEC) required clathrin to form actin-rich pedestals in host cells beneath adhering bacteria, even though this pathogen remains extracellular. Furthermore, clathrin accumulation preceded the actin rearrangements necessary for Listeria entry. These data provide evidence for a clathrin-based entry pathway allowing internalization of large objects (bacteria and ligand-coated beads) and used by "zippering" bacteria as part of a general mechanism to invade host mammalian cells. We also revealed a nonendocytic role for clathrin required for extracellular EPEC infections.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Bacteria / metabolism
  • Bacteria / pathogenicity*
  • Bacterial Adhesion / physiology*
  • Cell Line
  • Clathrin / physiology*
  • Dynamins / physiology
  • Endocytosis / physiology*
  • Enteropathogenic Escherichia coli / pathogenicity
  • Enteropathogenic Escherichia coli / physiology
  • Escherichia coli Infections / microbiology
  • Humans
  • Listeria monocytogenes / pathogenicity
  • Listeria monocytogenes / physiology
  • Listeriosis / microbiology
  • Receptors, Cell Surface / metabolism
  • Virulence


  • Actins
  • Clathrin
  • Receptors, Cell Surface
  • Dynamins