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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Involvement of CD44v6 in InlB-dependent Listeria invasion
C Jung1, A Matzke, H H Niemann
1Forschungszentrum Karlsruhe, Institute for Toxicology and Genetics, Postfach 3640, 76021 Karlsruhe, Germany.
Molecular Microbiology
|May 13, 2009
Summary
The bacterial protein InlB from Listeria monocytogenes activates host cell receptor c-Met for invasion. This process requires CD44v6, a transmembrane glycoprotein, and ezrin, highlighting a novel bacterial entry mechanism.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- Listeria monocytogenes causes listeriosis and invades host cells using surface proteins like E-cadherin and c-Met.
- Bacterial protein InlB activates c-Met, mimicking its natural ligand HGF, to facilitate host cell entry.
Purpose of the Study:
- To investigate the role of CD44v6 in InlB-mediated activation of c-Met.
- To elucidate the mechanism by which CD44v6 influences Listeria monocytogenes invasion.
Main Methods:
- Utilized blocking peptides, antibodies, and siRNA targeting CD44v6 to inhibit its function.
- Assessed c-Met phosphorylation, downstream signaling, and host cell invasion by InlB-coated beads.
- Investigated the involvement of ezrin in the CD44v6-mediated entry process.
Main Results:
- Inhibition of CD44v6 blocked InlB-induced c-Met activation, signaling, and host cell entry.
- Blocking CD44v6 significantly reduced Listeria monocytogenes invasion into host cells.
- Ezrin was found to be essential for the entry process, linking CD44v6 to the cytoskeleton.
Conclusions:
- CD44v6 is a critical co-receptor for InlB-mediated c-Met activation and Listeria monocytogenes invasion.
- The interaction between c-Met and CD44v6 represents a key pathway exploited by L. monocytogenes for cellular entry.
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