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Published ahead of print on January 31, 2003, doi:10.1164/rccm.200207-736BC

Am. J. Respir. Crit. Care Med., Volume 167, Number 11, June 2003, 1478-1482

A more recent version of this article appeared on June 1, 2003
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Submitted on July 23, 2002
Accepted on January 24, 2003

Role of the quorum-sensing system in experimental pneumonia due to Pseudomonas aeruginosa in rats

Philippe Lesprit1*, Francois Faurisson1, Olivier Join-Lambert1, Francoise Roudot-Thoraval2, Maryline Foglino3, Christiane Vissuzaine4, and Claude Carbon1

1 Institut National de la Sante et de la Recherche Medicale EMI-U 9933, Hopital Bichat, Paris, France, 2 Sante Publique, Hopital Henri Mondor, Creteil, Val de Marne, France, 3 Laboratoire d'Ingenierie des Systemes Macromoleculaires, Centre National de la Recherche Scientifique, Marseille, Bouches du Rhone, France, 4 Service d'Anatomie Pathologique, Hopital Bichat, Paris, France

* To whom correspondence should be addressed. E-mail: phillipe.lesprit{at}hmn.ap-hop-paris.fr.

Virulence of Pseudomonas aeruginosa is partly controlled by the las quorum-sensing (QS) system. A rat model of acute pneumonia was used to investigate the pathophysiological impact of this system by comparing the virulence of the wild-type virulent laboratory strain PAO1 and its lasR deleted mutant PAOR. In comparison with PAO1, PAOR was avirulent after an instillation of 106 CFU (mortality rates 72% vs 0% respectively, P &lt; 0.0001). A ten-fold higher inoculum slightly increased the mortality rate induced by PAOR (25%), which remained lower than that induced by PAO1 (75%, P = 0.0001). In addition, at both inocula lung and bronchoalveolar lavage bacterial counts were significantly lower in rats infected with PAOR than with PAO1 (P<=0.01). Histopathological analysis showed that PAO1 induced a drastic vascular congestion and neutrophil infiltration of the lungs,whereas lung injury in rats infected with PAOR was mild with predominant macrophage infiltration. This study adds evidence that the QS system has an important role in the pathophysiology of P. aeruginosa pulmonary infection.
Key words: cell-to cell signaling,experimental pneumonia,Pseudomonas aeruginosa




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