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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 normal host cell processes to spread from cell to cell

J R Robbins1, A I Barth, H Marquis

  • 1Department of Biochemistry, Stanford University School of Medicine, California 94305-5307, USA.

The Journal of Cell Biology
|September 24, 1999
PubMed

Insights

Listeria monocytogenes intercellular spread is hindered by cell-cell contacts. This bacterial pathogen may exploit host cell endocytosis for spread, a process termed paracytophagy.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Listeria monocytogenes is a bacterial pathogen that invades host cells.
  • Intercellular spread is a key virulence factor for L. monocytogenes, facilitated by actin-based motility.
  • The bacterial protein ActA is crucial for mediating actin-based motility and cell-to-cell spread.

Purpose of the Study:

  • To investigate the factors influencing intercellular spread of Listeria monocytogenes.
  • To characterize the dynamics of membrane-bound protrusions during bacterial spread.
  • To explore the potential role of host cell endocytosis in bacterial intercellular transmission.

Main Methods:

  • Infection of MDCK cell monolayers expressing GFP-actin with L. monocytogenes.
  • Live-cell video microscopy to observe bacterial spread and actin dynamics.
  • Analysis of membrane-bound protrusions and their interaction with host cells.

Main Results:

  • Intercellular spread probability decreased with host cell monolayer age and cell-cell contacts.
  • Bacterium-dependent movement of protrusions was observed, followed by vacuole formation and lysis.
  • Actin filaments in protrusions showed reduced turnover rates compared to cytoplasmic actin tails.
  • Recovery of bacterial motility in recipient cells was delayed (1-2 generations), potentially due to ActA cleavage by Mpl.
  • Host cell surface fragments were endocytosed in the absence of bacteria, suggesting paracytophagy.

Conclusions:

  • Host cell confluency and age negatively regulate Listeria monocytogenes intercellular spread.
  • Bacterial spread involves dynamic protrusions that collapse into vacuoles, leading to lysis.
  • Listeria monocytogenes may hijack host cell endocytic pathways, specifically paracytophagy, for efficient intercellular transmission.

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