How the parasitic bacterium Legionella pneumophila modifies its phagosome and transforms it into rough ER:

L G Tilney1, O S Harb, P S Connelly

  • 1Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA. kvranich@sas.upenn.edu

Journal of Cell Science
|January 17, 2002
PubMed

Insights

Legionella pneumophila hijacks host cell machinery, connecting to the rough endoplasmic reticulum (RER) and mitochondria early in infection. This bacterium manipulates phagosomal membranes to establish intracellular survival within the RER.

Area of Science:

  • Cell Biology
  • Microbiology
  • Infectious Diseases

Background:

  • Legionella pneumophila causes Legionnaires' disease, a severe pneumonia.
  • Intracellular pathogens often manipulate host cell processes for survival.
  • The interaction between L. pneumophila and host organelles is crucial for its pathogenesis.

Purpose of the Study:

  • To investigate the early interactions between Legionella pneumophila and host macrophage organelles.
  • To elucidate the mechanism by which L. pneumophila establishes intracellular residence.
  • To understand the role of the rough endoplasmic reticulum (RER) and mitochondria in L. pneumophila infection.

Main Methods:

  • Transmission electron microscopy of infected macrophages.
  • Analysis of phagosome-organelle connections using thin sections.
  • Examination of L. pneumophila mutants to dissect the infection stages.

Main Results:

  • Within minutes, L. pneumophila phagosomes associate with RER and mitochondria via stable, high-affinity connections.
  • Phagosomal membrane composition and thickness change to resemble RER membranes.
  • L. pneumophila eventually resides within the RER, suggesting a four-stage process of host cell manipulation.

Conclusions:

  • L. pneumophila actively remodels its phagosomal environment by recruiting and integrating with host RER and mitochondria.
  • The bacterium exploits a natural cellular process to achieve intracellular survival and replication.
  • This study reveals a sophisticated mechanism of host-pathogen interaction essential for Legionnaires' disease pathogenesis.

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