Fig. 1.

Flagellar motility is a key bacterial determinant for phagocytic susceptibility of Pseudomonas aeruginosa by both murine and human phagocytes, with motile bacteria phagocytosed ∼100-fold more efficiently than nonmotile bacteria (top). Although the cell surface phagocytic receptor(s) for P. aeruginosa require further elucidation, independent reports indicate that bacterial engulfment is actin dependent and controlled by the PI3K/Akt signaling pathway. P. aeruginosa has also been proposed to invade epithelial cells (bottom), particularly on the basolateral surfaces of these cells, through alterations in cell polarity and in breaches in the monolayer. Proposed mechanisms include invasion via cell surface lipid rafts in conjunction with the caveolin-2 protein, and via heparin sulfate proteoglycans (HSPGs). The HSPG-mediated pathway is subsequently dependent on intracellular PI3K/Akt activity, and RhoA and/or Cdc42 activation. The relationship between the HSPG and lipid raft-mediated pathways is currently unclear.