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Published ahead of print on January 31, 2003, doi:10.1164/rccm.200207-736BC
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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 1478-1482, (2003)
© 2003 American Thoracic Society

Brief Communication

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

Philippe Lesprit, François Faurisson, Olivier Join-Lambert, Françoise Roudot-Thoraval, Maryline Foglino, Christiane Vissuzaine and Claude Carbon

INSERM EMI-U 9933, and Service d'Anatomie Pathologique, Hôpital Bichat, Paris, France; Département de Santé Publique, Hôpital Henri Mondor, Créteil; and Laboratoire d'Ingénierie des Systèmes Macromoléculaires, Centre National de la Recherche Scientifique, Marseille, France

Correspondence and requests for reprints should be addressed to Dr. Philippe Lesprit, Service d'Immunologie Clinique, Hôpital Henri Mondor, 51 avenue du Maréchal de Lattre, 94010 Créteil, France. E-mail: phillipe.lesprit{at}hmn.ap-hop-paris.fr

The virulence of Pseudomonas aeruginosa is partly controlled by the las quorum-sensing 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 with that of its lasR-deleted mutant PAOR. In comparison with PAO1, PAOR was avirulent after an instillation of 106 cfu (mortality rates, 72 versus 0%, respectively; p < 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, with 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 predominantly macrophage infiltration. This study adds evidence that the quorum-sensing 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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