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Production of exopolysaccharide by Burkholderia cenocepacia results in altered cell-surface interactions and altered bacterial clearance in mice

Journal article
Authors B. A. Conway
K. K. Chu
Johan Bylund
E. Altman
D. P. Speert
Published in J Infect Dis
Volume 190
Issue 5
Pages 957-66
Publication year 2004
Published at Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
Pages 957-66
Language en
Keywords 4-Butyrolactone/analogs & derivatives/biosynthesis, Animals, Bacterial Capsules/*metabolism, Biofilms/growth & development, Burkholderia Infections/immunology/microbiology, Burkholderia cepacia complex/classification/*growth &, development/isolation & purification/*pathogenicity, Cystic Fibrosis/*immunology/*microbiology, Disease Models, Animal, Electrophoresis, Gel, Pulsed-Field, Female, Humans, Mice, Mice, Inbred BALB C, Random Amplified Polymorphic DNA Technique
Subject categories Medical and Health Sciences


Despite the characterization of some Burkholderia cepacia complex exopolysaccharides (EPSs), little is known about the role of EPSs in the pathogenicity of B. cepacia complex organisms. We describe 2 Burkholderia cenocepacia (genomovar III) isolates obtained from a patient with cystic fibrosis (CF): the nonmucoid isolate C8963 and the mucoid isolate C9343. Both isolates had identical random amplified polymorphic DNA patterns. C9343 produced a capsule composed of the EPSs PS-I and PS-II, as well as alpha -1,6-glucan. These isolates exhibited several phenotypic differences: C8963 synthesized octanoyl-homoserine lactone and produced biofilms, but C9343 did not; in a mouse model of pulmonary infection, C8963 was cleared more rapidly than was C9343; and C9343 interacted poorly with macrophages and neutrophils, compared with C8963, suggesting that the C9343 capsule interfered with cell-surface interactions. Overproduction of EPS by C9343 resulted in a mucoid appearance and interfered with cell-surface interactions and clearance in an animal model. This mucoid colonial appearance could enhance the persistence and virulence of this important CF-related pathogen.

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