IAI Accepts, published online ahead of print on 23 February 2009

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Infect. Immun. doi:10.1128/IAI.01204-08
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Role of LecA and LecB lectins in Pseudomonas aeruginosa induced lung injury and effect of carbohydrates ligands

Chanez Chemani, Anne Imberty, Sophie de Bentzman, Maud Pierre, Michaela Wimmerová, Benoît P Guery^*, and Karine Faure

EA 2689, IFR 114, Faculté de Médecine, Université de Lille 2 and CHRU de Lille, France; CERMAV-CNRS, Grenoble, France; UPR9027 CNRS, IFR88, Systèmes membranaires et pathogénicité chez Pseudomonas aeruginosa, Marseille, France; EA 3925, IFR 114, Clinique de Pédiatrie, Hôpital Jeanne de Flandre, Université de Lille 2 and CHRU de Lille, France; NCBR and Department of Biochemistry, Masaryk University, Brno, Czech Republic

^* To whom correspondence should be addressed. Email: bguery{at}invivo.edu.

Pseudomonas aeruginosa is a frequently encountered pathogen involved in acute and chronic lung infections. Lectin-mediated bacterial-cellular recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the respective contribution of LecA and LecB in the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model on A549 cells, and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA and Lec B-specific lectin inhibiting carbohydrates (-methyl-galactoside and -methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. Bacterial burden and dissemination decreased for both mutants compared to the parental strain. Co-administration of specific lectins inhibitors markedly prevented lung injury and mortality. Our results demonstrate a relationship between lectins and pathogenicity of P. aeruginosa. The inhibition of these lectins by specific carbohydrates may offer new therapeutic perspectives.

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