Role of the Quorum-sensing System in Experimental Pneumonia due to Pseudomonas aeruginosa in Rats

The virulence of Pseudomonas aeruginosa is partly controlled by the and is required for optimal production of LasA and LasB elaslas quorum-sensing system. A rat model of acute pneumonia was tases, alkaline protease, exotoxin A, and proteins of the secreused to investigate the pathophysiological impact of this system tory pathway (3). The second signaling system, referred to as by comparing the virulence of the wild-type virulent laboratory rhl (for rhamnolipid production), is also necessary for optimal strain PAO1 with that of its lasR-deleted mutant PAOR. In compari- production of elastases, protease, pyocyanin, and hemolysin (4). son with PAO1, PAOR was avirulent after an instillation of 10 6 cfu Although both systems are highly specific for their respective (mortality rates, 72 versus 0%, respectively; p 0.0001). A ten- autoinducers, there is a QS signaling hierarchy, because the las fold higher inoculum slightly increased the mortality rate induced system activates the expression of rhlR/rhlI. In vitro studies by PAOR (25%), which remained lower than that induced by PAO1 have shown that production of elastase and other virulence (75%, p 0.0001). In addition, with both inocula lung and bron- factors are reduced in P. aeruginosa mutants defective in the choalveolar lavage bacterial counts were significantly lower in rats las or the rhl systems (3, 5), but only a few studies have coninfected with PAOR than with PAO1 (p 0.01). Histopathological firmed this role in vivo. analysis showed that PAO1 induced a drastic vascular congestion The aim of this study was to determine the role of QS in and neutrophil infiltration of the lungs, whereas lung injury in rats the physiopathology of acute pulmonary infection by comparing infected with PAOR was mild with predominantly macrophage infilthe wild-type laboratory strain P. aeruginosa PAO1, which postration. This study adds evidence that the quorum-sensing system