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J. Biol. Chem., Vol. 281, Issue 5, 2526-2532, February 3, 2006

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Exopolysaccharides from Burkholderia cenocepacia Inhibit Neutrophil Chemotaxis and Scavenge Reactive Oxygen Species^*

Johan Bylund¹, Lee-Anna Burgess, Paola Cescutti, Robert K. Ernst^¶, and David P. Speert²

From the Department of Pediatrics, University of British Columbia, Child and Family Research Institute, Vancouver, British Columbia V5Z 4H4, Canada, the Department of Biochemistry, Biophysics and Macromolecular Chemistry, University of Trieste, 34127 Trieste, Italy, and the ^¶Department of Medicine, University of Washington, Seattle, Washington 98195

Bacteria belonging to the Burkholderia cepacia complex are important opportunistic pathogens in compromised hosts, particularly patients with cystic fibrosis or chronic granulomatous disease. Isolates of B. cepacia complex may produce large amounts of exopolysaccharides (EPS) that endow the bacteria with a mucoid phenotype and appear to facilitate bacterial persistence during infection. We showed that EPS from a clinical B. cenocepacia isolate interfered with the function of human neutrophils in vitro; it inhibited chemotaxis and production of reactive oxygen species (ROS), both essential components of innate neutrophil-mediated host defenses. These inhibitory effects were not due to cytotoxicity or interference with intracellular calcium signaling. EPS also inhibited enzymatic generation of ROS in cell-free systems, indicating that it scavenges these bactericidal products. B. cenocepacia EPS is structurally distinct from Pseudomonas aeruginosa alginate, yet they share the capacity to scavenge ROS and inhibit chemotaxis. These properties could explain why the two bacterial species resist clearance from the infected cystic fibrosis lung.

Received for publication, September 30, 2005 , and in revised form, November 14, 2005.

^* This study was funded by grants from the Canadian Cystic Fibrosis Foundation (to J. B., L.-A. B., and D. P. S.), Cystic Fibrosis Foundation (to R. K. E.), National Institutes of Health (Grant U54AI057141) (to R. K. E.), the Swedish Society for Medical Research (to J. B.), and the Canadian Institute for Health Research (to D. P. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Present address: Dept. of Rheumatology and Inflammation Research, University of Göteborg, Göteborg, Sweden.

² To whom correspondence should be addressed: Dept. of Pediatrics, University of British Columbia, Child and Family Research Institute, Rm. 377, 950 West 28th Ave., Vancouver, B. C., V5Z 4H4, Canada. Tel.: 604-875-2438; Fax: 604-875-2226; E-mail: dspeert{at}cw.bc.ca.

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