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Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
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Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes

Published on: August 9, 2011

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InIB-dependent internalization of Listeria is mediated by the Met receptor tyrosine kinase

Y Shen1, M Naujokas, M Park

  • 1Department of Medical Genetics and Microbiology, University of Toronto, Ontario, Canada.

Cell
|November 18, 2000
PubMed

Insights

The Listeria monocytogenes surface protein InlB hijacks the host Met receptor tyrosine kinase (RTK) to promote bacterial invasion. This study identifies Met as the cellular receptor essential for InlB-mediated entry into mammalian cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Molecular Biology

Background:

  • Listeria monocytogenes is an intracellular pathogen that invades host cells.
  • The surface protein InlB facilitates bacterial entry into mammalian cells.
  • The specific host cell receptor for InlB-mediated entry was previously unknown.

Purpose of the Study:

  • To identify the cellular surface receptor utilized by InlB for bacterial entry.
  • To elucidate the mechanism by which InlB mediates invasion.
  • To characterize the interaction between InlB and its host receptor.

Main Methods:

  • Treatment of mammalian cells with InlB protein and L. monocytogenes infection.
  • Analysis of tyrosine phosphorylation of Met, a receptor tyrosine kinase (RTK).
  • Experiments using Met-positive and Met-deficient cell lines.

Main Results:

  • InlB binding to Met induces tyrosine phosphorylation and epithelial cell scattering, similar to Hepatocyte Growth Factor (HGF).
  • Met was found to be essential for InlB-dependent entry of L. monocytogenes.
  • InlB acts as a novel Met agonist.

Conclusions:

  • Met is the cellular receptor required for InlB-mediated entry of Listeria monocytogenes.
  • InlB exploits the host Met receptor tyrosine kinase pathway to facilitate bacterial invasion.
  • This identifies a novel mechanism of host-pathogen interaction and bacterial entry.

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