Pharmacological activation of Rap1 antagonizes the endothelial barrier disruption induced by exotoxins ExoS and ExoT of Pseudomonas aeruginosa.

ABSTRACT: Most clinical strains of Pseudomonas aeruginosa, a leading agent of nosocomial infections, are multiresistant to antibiotherapy. Because of the paucity of new available antibiotics, the investigation of strategies aimed at limiting the action of its major virulence factors has gained much interest. The type 3 secretion system of P. aeruginosa and its effectors are known to be major determinants of toxicity and are required for bacterial dissemination in the host. Bacterial transmigration across the vascular wall is considered to be an important step in the infectious process. Using human endothelial primary cells, we demonstrate that forskolin (FSK), a drug inducing cyclic AMP (cAMP) elevation in eukaryotic cells, strikingly reduced the cell retraction provoked by two type 3 toxins, ExoS a

SUBMITTER: Bouillot S 

PROVIDER: S-EPMC4399046 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature