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Published on: October 15, 2013

Burkholderia cenocepacia disrupts host cell actin cytoskeleton by inactivating Rac and Cdc42

Ronald S Flannagan1, Valentin Jaumouillé, Kassidy K Huynh

  • 1Program in Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8.

Cellular Microbiology
|October 26, 2011
PubMed

Insights

Burkholderia cenocepacia evades immune cells by disrupting macrophage actin cytoskeleton. This pathogen inactivates Rho GTPases, impairing phagocyte function and enabling survival within host cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Burkholderia cenocepacia is an opportunistic pathogen causing severe infections in cystic fibrosis patients.
  • B. cenocepacia's intracellular survival mechanisms are crucial for its virulence, especially in immunocompromised individuals.

Purpose of the Study:

  • To investigate the mechanisms by which B. cenocepacia survives within macrophages.
  • To understand how B. cenocepacia manipulates host cell functions to promote its intracellular persistence.

Main Methods:

  • Infection of macrophages with B. cenocepacia.
  • Analysis of actin cytoskeleton dynamics and host cell morphology.
  • Assessment of Rho family GTPase activity (Rac1, Cdc42).
  • Evaluation of phagocytosis and macropinocytosis inhibition.
  • Investigation of the role of the type VI secretion system.

Main Results:

  • B. cenocepacia disrupts the macrophage actin cytoskeleton, causing cell retraction.
  • The bacteria inactivate Rho family GTPases (Rac1, Cdc42), compromising phagocyte function.
  • Macropinocytosis and phagocytosis are significantly inhibited in infected macrophages.
  • The type VI secretion system is essential for B. cenocepacia to induce these cellular changes.

Conclusions:

  • B. cenocepacia employs a novel mechanism involving Rho GTPase inactivation to survive within macrophages.
  • This inactivation impairs crucial macrophage functions, contributing to the pathogen's virulence.
  • The type VI secretion system plays a key role in mediating these host cell manipulations.

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