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Related Experiment Videos

Stalling autophagy: a new function for Listeria phospholipases.

Ivan Tattoli1, Matthew T Sorbara2, Dana J Philpott2

  • 1Department of Laboratory Medicine and Pathobiology, University of Toronto, M6G 2T6, Toronto, Canada. ; Department of Immunology, University of Toronto, M6G 2T6, Toronto, Canada.

Microbial Cell (Graz, Austria)
|March 31, 2017
PubMed
Summary

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Listeria monocytogenes phospholipases PI-PLC and PC-PLC aid bacterial escape from host cell autophagy. These toxins inhibit autophagic flux, facilitating intracellular survival and spread.

Area of Science:

  • Bacteriology
  • Cell Biology
  • Infectious Diseases

Background:

  • Listeria monocytogenes invades host cells and escapes vacuoles using listeriolysin O (LLO).
  • L. monocytogenes also secretes PI-PLC and PC-PLC phospholipases, aiding vacuole escape and cell-to-cell spread.
  • The role of these phospholipases during the cytosolic stage of infection was previously uncharacterized.

Purpose of the Study:

  • To investigate the role of Listeria monocytogenes PI-PLC and PC-PLC during the cytosolic stage of infection.
  • To determine if these phospholipases play a role in bacterial escape from host cell autophagy.

Main Methods:

  • The study likely involved bacterial infection models in cell culture.
  • Investigated the interaction of L. monocytogenes phospholipases with the host autophagy pathway.
Keywords:
AutophagyListeriamTOR

Related Experiment Videos

  • Assessed the impact of phospholipase activity on autophagic flux and bacterial survival.
  • Main Results:

    • L. monocytogenes PI-PLC and PC-PLC were found to contribute to bacterial escape from autophagy.
    • These phospholipases were shown to directly inhibit the autophagic flux in infected host cells.
    • This inhibition facilitates bacterial survival and replication within the host cell cytosol.

    Conclusions:

    • Listeria monocytogenes phospholipases PI-PLC and PC-PLC have a novel role in evading host immune responses.
    • By inhibiting autophagic flux, these toxins promote bacterial intracellular survival and pathogenesis.
    • Targeting these phospholipases could represent a potential strategy for treating L. monocytogenes infections.