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Listeria monocytogenes Infection of the Brain
05:02

Listeria monocytogenes Infection of the Brain

Published on: October 2, 2018

Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell

Sascha Pust1, Helen Morrison, Jürgen Wehland

  • 1Department of Cell Biology, Gesellschaft für Biotechnologische Forschung (GBF), Braunschweig, Germany.

The EMBO Journal
|February 25, 2005
PubMed

Insights

Listeria monocytogenes uses ezrin, a membrane-cytoskeleton linker, to form protrusions for cell-to-cell spread. Disrupting ezrin interactions impairs Listeria infection by hindering protrusion formation.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Cell-to-cell spread is crucial for Listeria monocytogenes infection.
  • This spread relies on bacteria-induced protrusions, which involve actin tails linked to the plasma membrane.

Purpose of the Study:

  • To investigate the role of membrane-cytoskeleton linkers in Listeria monocytogenes protrusion formation and cell-to-cell spread.
  • To identify specific proteins involved in linking the plasma membrane to the actin cytoskeleton during infection.

Main Methods:

  • Immunofluorescence microscopy to observe ezrin localization at Listeria protrusions.
  • Genetic and biochemical approaches to disrupt ezrin interactions with CD44 and actin.
  • Assessment of protrusion formation and Listeria cell-to-cell spread efficiency.

Main Results:

  • Ezrin, a key ezrin, radixin, and moesin (ERM) family protein, was found to accumulate at Listeria protrusions.
  • ERM protein interaction with CD44 and actin filaments is essential for inducing protrusions and Listeria spread.
  • Interference with ERM protein interactions or phosphorylation led to reduced and abnormal protrusion formation, severely impairing cell-to-cell spread.

Conclusions:

  • Ezrin and other ERM proteins are critical host factors exploited by Listeria monocytogenes for efficient cell-to-cell spread.
  • Targeting ERM protein function could be a strategy to control Listeria infections.
  • This study elucidates a novel mechanism of host-pathogen interaction essential for Listeria pathogenesis.

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