Disease relevance of Burkholderia

• We have found that mannose-binding lectin binds to Burkholderia cepacia, an important pathogen in patients with cystic fibrosis, and leads to complement activation, but that this is not the case for Pseudomonas aeruginosa, the more common colonising organism in this disease [1].
• Catalase-peroxidases (KatG) produced by Burkholderia pseudomallei, Escherichia coli, and Mycobacterium tuberculosis catalyze the oxidation of NADH to form NAD+ and either H2O2 or superoxide radical depending on pH [2].
• The fold adopted by the 392-amino acid polypeptide generated a two-domain structure that is similar to the folds of the penicillin-recognizing family of serine-reactive hydrolases, especially to those of d-alanyl-d-alanine-carboxypeptidase from Streptomyces and carboxylesterase from Burkholderia [3].
• P450 PFOR genes are found in a Rhodococcus strain, three pathogenic Burkholderia species and in the R. metallidurans strain that possesses a P450 BM3 homologue [4].
• The Burkholderia cepacia complex is an important group of pathogens in patients with cystic fibrosis (CF) [5].

High impact information on Burkholderia

• Salicylate induces an antibiotic efflux pump in Burkholderia cepacia complex genomovar III (B. cenocepacia) [6].
• Burkholderia cepacia and nebulized albuterol [7].
• The distribution of aqueous Pb(II) sorbed at the interface between Burkholderia cepacia biofilms and hematite (alpha-Fe(2)O(3)) or corundum (alpha-Al(2)O(3)) surfaces has been probed by using an application of the long-period x-ray standing wave technique [8].
• The purified protein catalyzed the NADPH-dependent reduction of the carbon-carbon double bond of 2-chloroacrylate to produce (S)-2-chloropropionate, which is probably further metabolized to (R)-lactate by (S)-2-haloacid dehalogenase in Burkholderia sp. WS. NADH did not serve as a reductant [9].
• 2,2'-Dichlorobiphenyl (CB) is transformed by the biphenyl dioxygenase of Burkholderia xenovorans LB400 (LB400 BPDO) into two metabolites (1 and 2) [10].

Chemical compound and disease context of Burkholderia

• Identification, characterization, and cloning of a phosphonate monoester hydrolase from Burkholderia caryophilli PG2982 [11].
• The ability of 2-hydroxy-6-oxo-6-phenylhexa-2,4-dienoate (HOPDA) hydrolase (BphD) of Burkholderia cepacia LB400 to hydrolyze polychlorinated biphenyl (PCB) metabolites was assessed by determining its specificity for monochlorinated HOPDAs [12].
• Revisiting the regiospecificity of Burkholderia xenovorans LB400 biphenyl dioxygenase toward 2,2'-dichlorobiphenyl and 2,3,2',3'-tetrachlorobiphenyl [10].
• The glyphosate-degrading bacterium, Burkholderia caryophilli PG2982, was observed to utilize glyceryl glyphosate as a sole phosphorus source [11].
• Quorum sensing and the LysR-type transcriptional activator ToxR regulate toxoflavin biosynthesis and transport in Burkholderia glumae [13].

Biological context of Burkholderia

• Evolution of the biphenyl dioxygenase BphA from Burkholderia xenovorans LB400 by random mutagenesis of multiple sites in region III [14].
• Pyochelin is a siderophore and virulence factor common to Burkholderia cepacia and several Pseudomonas strains [15].
• CpG-modified plasmid DNA encoding flagellin improves immunogenicity and provides protection against Burkholderia pseudomallei infection in BALB/c mice [16].
• Assignment of the 1H, 13C and 15N resonances of the catalytic domain of guanine nucleotide exchange factor BopE from Burkholderia pseudomallei [17].
• The Burkholderia pseudomallei K96243 genome contains multiple type IV pilin-associated loci, including one encoding a putative pilus structural protein (pilA) [18].

Anatomical context of Burkholderia

• We evaluated the activities of meropenem, imipenem, temocillin, piperacillin, and ceftazidime by determination of the MICs for 66 genotypically characterized Burkholderia cepacia isolates obtained from the sputum of cystic fibrosis patients [19].
• Cable-piliated Burkholderia cepacia binds to cytokeratin 13 of epithelial cells [20].
• Lipopolysaccharide of Burkholderia cepacia and its unique character to stimulate murine macrophages with relative lack of interleukin-1beta-inducing ability [21].
• Phagocyte NADPH oxidase, but not inducible nitric oxide synthase, is essential for early control of Burkholderia cepacia and chromobacterium violaceum infection in mice [22].
• Of 56 samples from ethacridine lactate solutions (eight products, seven manufacturers), seven samples (12.5%) of two products (two manufacturers) were contaminated with 10(1)-10(4) colony forming units (cfu)/mL of Burkholderia pickettii [23].

Gene context of Burkholderia

• We found that abundant airway antimicrobial factors kill common CF pathogens, although Burkholderia was relatively resistant [24].
• Caspase-1 dependent macrophage death induced by Burkholderia pseudomallei [25].
• Actin-based motility of Burkholderia pseudomallei involves the Arp 2/3 complex, but not N-WASP and Ena/VASP proteins [26].
• Burkholderia sacchari IPT101(T) induced the formation of 2-methylcitrate synthase and 2-methylisocitrate lyase when it was cultivated in the presence of propionic acid [27].
• An hrpXv mutant could be partially complemented by the related hrpB gene of Burkholderia solanacearum, the protein product of which shows 40 and 58% amino acid identity and similarity, respectively, to HrpXv [28].

Analytical, diagnostic and therapeutic context of Burkholderia

• As a result of concern over excessive mortality after lung transplantation, many transplant programs refuse to accept cystic fibrosis (CF) patients infected with Burkholderia cepacia [29].
• Development of a 5'-nuclease real-time PCR assay targeting fliP for the rapid identification of Burkholderia mallei in clinical samples [30].
• The cell-associated glucans produced by Burkholderia solanacearum and Xanthomonas campestris pv. citri were isolated by trichloroacetic acid treatment and gel permeation chromatography [31].
• Home-use nebulizers: a potential primary source of Burkholderia cepacia and other colistin-resistant, gram-negative bacteria in patients with cystic fibrosis [32].
• lux-marked biosensors for assessing the toxicity and bioremediation potential of polluted environments may complement traditional chemical techniques. luxCDABE genes were introduced into the chromosome of the 2,4-dichlorophenol (2,4-DCP)-mineralizing bacterium, Burkholderia sp. RASC c2, by biparental mating using the Tn4431 system [33].

References