Abstract
Introduction The Burkholderia cepacia complex (Bcc) comprises about 17 related opportunistic pathogens that are able to infect the respiratory tract of cystic fibrosis (CF) patients and chronic granulomatous disease patients [1]. It has also been reported as a cause of bacteraemia [2]. Up to 8% of patients are colonized by Bcc
Highlights
The Burkholderia cepacia complex (Bcc) comprises about 17 related opportunistic pathogens that are able to infect the respiratory tract of cystic fibrosis (CF) patients and chronic granulomatous disease patients [1]
Bacterial strains and growth conditions The bacterial strains used in this work were the wild type strain B. cenocepacia J2315 and the mutant D4 harbouring a deletion of the two ORF BCAL2822–BCAL2820 (RND-4) [12]
In order to establish the cellular processes affected by the ResistanceNodulation-Cell Division (RND)-4 multidrug efflux pump gene deletion in
Summary
The Burkholderia cepacia complex (Bcc) comprises about 17 related opportunistic pathogens that are able to infect the respiratory tract of cystic fibrosis (CF) patients and chronic granulomatous disease patients [1] It has been reported as a cause of bacteraemia [2]. Among the mechanisms of resistance, enzymatic inactivation as well as alteration of drug target and cell wall permeability, has been reported [7] Another aspect related to drug resistance is the presence in the of B. cenocepacia genome of genes encoding all five major families of efflux systems [8]. The Burkholderia cenocepacia J2315 is Gram-negative bacterium that is a pathogen for cystic fibrosis (CF) patients It displays a high-level of resistance to most antimicrobial drugs. The aim of this study was to investigate the role of this efflux transporter from a proteomic point of view
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