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Microbiology 153 (2007), 2312-2320; DOI  10.1099/mic.0.2007/006122-0
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Microbiology 153 (2007), 2312-2320; DOI  10.1099/mic.0.2007/006122-0
© 2007 Society for General Microbiology

Impact of Pseudomonas aeruginosa quorum sensing on biofilm persistence in an in vivo intraperitoneal foreign-body infection model

Louise D. Christensen1, Claus Moser2, Peter Ø. Jensen2, Thomas B. Rasmussen3, Lars Christophersen2, Staffan Kjelleberg4, Naresh Kumar5, Niels Høiby2, Michael Givskov1 and Thomas Bjarnsholt1

1 Bioscience and Technology, BioCentrum, Technical University of Denmark, DK-2800 Lyngby, Denmark
2 Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark
3 Genomics and Strain Development, Chr. Danish Hansen A/S, Bøge Alle 10-12, DK-2970, Hørsholm, Denmark
4 Center for Marine Biofouling and Bioinnovation, University of New South Wales, NSW 2052, Australia
5 School of Chemistry, University of New South Wales, NSW 2052, Australia

Correspondence
Thomas Bjarnsholt
tbj{at}biocentrum.dtu.dk

Pseudomonas aeruginosa is an opportunistic human pathogen that causes chronic biofilm-based infections in host organisms. P. aeruginosa employs quorum sensing (QS) to control expression of its virulence, and to establish and maintain chronic infections. Under such conditions, the biofilm mode of growth contributes significantly to P. aeruginosa tolerance to the action of the innate and adaptive defence system and numerous antibiotics. In the present study, an in vivo foreign-body infection model was established in the peritoneal cavity of mice. Experimental data showed that QS-deficient P. aeruginosa are cleared more rapidly from silicone implants as compared to their wild-type counterparts. Concurrently, treatment with the QS inhibitor furanone C-30 of mice harbouring implants colonized with the wild-type P. aeruginosa resulted in a significantly faster clearing of the implants as compared to the placebo-treated group. These results were obtained with both an inbred (BALB/c) and an outbred (NMRI) mouse strain. The present results support a model by which functional QS systems play a pivotal role in the ability of bacteria to resist clearing by the innate immune system and strongly suggest that the efficiency of the mouse innate defence against biofilm-forming P. aeruginosa is improved when the bacteria are treated with QS drugs that induce QS deficiency.


Abbreviations: AHL, N-acyl-L-homoserine lactone; BAL, bronchoalveolar lavage; C4-HSL, N-butanoyl-L-homoserine lactone; CLSM, confocal laser scanning microscopy; GFP, green fluorescent protein; 3-oxo-C12-HSL, N-(3-oxododecanoyl)-L-homoserine lactone; PMN, polymorphonuclear leukocyte; PQS, Pseudomonas quinolone signal; QS, quorum sensing




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