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Regulation of Rab5 function during phagocytosis of live Pseudomonas aeruginosa in macrophages

Sushmita Mustafi1, Nathalie Rivero, Joan C Olson

  • 1Department of Biological Sciences, Florida International University, Miami, Florida, USA.

Infection and Immunity
|May 1, 2013
PubMed

Insights

Pseudomonas aeruginosa uses its ExoS effector to inhibit macrophage phagocytosis by inactivating Rab5. This bacterial manipulation of host cell processes is key to P. aeruginosa infections.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Pseudomonas aeruginosa is a Gram-negative bacterium causing hospital-acquired infections.
  • Type III secretion system effectors, like ExoS, disrupt host cell functions.
  • ExoS targets host proteins, including Ras and Rab GTPases, impacting cell signaling and trafficking.

Purpose of the Study:

  • To investigate the role of Rab5 in Pseudomonas aeruginosa invasion of macrophages.
  • To determine how P. aeruginosa manipulates Rab5 activity during infection.
  • To identify the specific P. aeruginosa effector responsible for Rab5 regulation.

Main Methods:

  • Utilized J774-Eclone macrophages and live/heat-inactivated P. aeruginosa.
  • Assessed phagocytosis inhibition and Rab5 activity.
  • Investigated the role of ExoS ADP-ribosyltransferase and Rho GTPase activities.
  • Examined the effect of Rin1, Rabex5, and Rap6 on Rab5 activity.

Main Results:

  • Live P. aeruginosa inhibited macrophage phagocytosis, correlating with Rab5 activity downregulation.
  • ExoS ADP-ribosyltransferase activity was responsible for Rab5 inactivation.
  • ExoS ADP-ribosyltransferase activity caused more significant phagocytosis inhibition than ExoS Rho GTPase activity.
  • Rin1 partially reversed Rab5 inactivation during P. aeruginosa invasion.

Conclusions:

  • Rab5 is critical for early P. aeruginosa invasion of macrophages.
  • P. aeruginosa directly regulates Rab5 activation to control phagocytosis.
  • The ExoS effector plays a key role in modulating host cell processes for bacterial advantage.

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