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Related Experiment Videos

Rho GTPase activity modulates Pseudomonas aeruginosa internalization by epithelial cells.

B I Kazmierczak1, T S Jou, K Mostov

  • 1Department of Medicine, University of California, San Francisco 94143-0654, USA.

Cellular Microbiology
|February 24, 2001
PubMed
Summary
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Pseudomonas aeruginosa internalization into epithelial cells is stimulated by RhoA activation, but not inhibited by RhoA blockade. This suggests RhoA plays a complex role in bacterial invasion pathways.

Area of Science:

  • Microbiology
  • Cell Biology
  • Bacterial Pathogenesis

Background:

  • *Pseudomonas aeruginosa* is a Gram-negative pathogen that invades host epithelial cells.
  • Bacterial internalization pathways are actin-dependent and involve Rho family GTPases.
  • Epithelial cell polarization affects bacterial internalization, suggesting a role for Rho GTPases.

Purpose of the Study:

  • To investigate the role of Rho family GTPases in *Pseudomonas aeruginosa* internalization into epithelial cells.
  • To determine if RhoA, Rac1, or Cdc42 mediate bacterial uptake.
  • To elucidate the mechanism by which *P. aeruginosa* invades epithelial cells.

Main Methods:

  • *Pseudomonas aeruginosa* strain PA103 internalization assays in Madin-Darby canine kidney (MDCK) cells.

Related Experiment Videos

  • Stimulation of Rho family GTPases using cytotoxic necrotizing factor 1 (CNF-1).
  • Expression of constitutively active and dominant-negative Rho GTPase alleles.
  • Inhibition of actin polymerization with latrunculin A.
  • Measurement of endogenous Rho GTP levels during bacterial infection.

    • Main Results:

    • Activation of Rho family GTPases by CNF-1 stimulates *P. aeruginosa* internalization.
    • Constitutively active RhoA (RhoAV14) increases bacterial uptake, while Rac1 and Cdc42 do not.
    • RhoAV14-mediated uptake is actin-dependent and not solely due to tight junction disruption.
    • Infection with invasive *P. aeruginosa* increases endogenous Rho GTP levels, while non-invasive strains decrease them.
    • Experimental inhibition of Rho does not prevent bacterial internalization.

    Conclusions:

    • RhoA activation, but not inhibition, promotes *P. aeruginosa* internalization.
    • RhoA plays a complex role in bacterial invasion, potentially involving both promotion and regulation.
    • The findings provide insights into the host cell mechanisms exploited by *P. aeruginosa* for invasion.