Pseudomonas aeruginosa is an opportunistic pathogen responsible for severe pulmonary infections in debilitated

patients hospitalized in ICU or suffering from cystic fibrosis. Infections caused by P. aeruginosa are difficult to treat due to (i) the remarkable ability of the pathogen to express constitutive and inducible resistance mechanisms (low permeability of the outer membrane, efflux pumps [over]expression, enzymatic inactivation of antibiotics) and (ii) its ability to enter and survive in eucaryotic cells, where the efficacy of antibiotics is considerably reduced [1]. Discovering novel antibacterial agents acting on unexploited targets is critically needed to cope with infections caused by multiresistant organisms [2]. Exploring their cellular pharmacokinetics and pharmacodynamics may help t