Ionizing groups in lipopolysaccharides of <i>Pseudomonas cepacia</i> in relation to antibiotic resistance

Cox, Andrew D.; Wilkinson, Stephen G.

doi:10.1111/j.1365-2958.1991.tb00735.x

Cited by 97 publications

(72 citation statements)

References 42 publications

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“…The structure and composition of B. cenocepacia LPS contributes to the intrinsic resistance to aminoglycoside (30,91) and polymyxin. The presence of 4-amino-4-deoxy-L-arabinose moieties within the inner core region has been shown to reduce the binding of cationic antibiotics such as polymyxin B to B. cenocepacia LPS (74,122).…”

Section: Lps and Exopolysaccharide (Eps)mentioning

confidence: 99%

The Genome of Burkholderia cenocepacia J2315, an Epidemic Pathogen of Cystic Fibrosis Patients

et al. 2009

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Bacterial infections of the lungs of cystic fibrosis (CF) patients cause major complications in the treatment of this common genetic disease.Burkholderia cenocepacia infection is particularly problematic since this organism has high levels of antibiotic resistance, making it difficult to eradicate; the resulting chronic infections are associated with severe declines in lung function and increased mortality rates. B. cenocepacia strain J2315 was isolated from a CF patient and is a member of the epidemic ET12 lineage that originated in Canada or the United Kingdom and spread to Europe. The 8.06-Mb genome of this highly transmissible pathogen comprises three circular chromosomes and a plasmid and encodes a broad array of functions typical of this metabolically versatile genus, as well as numerous virulence and drug resistance functions. Although B. cenocepacia strains can be isolated from soil and can be pathogenic to both plants and man, J2315 is representative of a lineage of B. cenocepacia rarely isolated from the environment and which spreads between CF patients. Comparative analysis revealed that ca. 21% of the genome is unique in comparison to other strains of B. cenocepacia, highlighting the genomic plasticity of this species. Pseudogenes in virulence determinants suggest that the pathogenic response of J2315 may have been recently selected to promote persistence in the CF lung. The J2315 genome contains evidence that its unique and highly adapted genetic content has played a significant role in its success as an epidemic CF pathogen.

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Section: Lps and Exopolysaccharide (Eps)mentioning

confidence: 99%

The Genome of Burkholderia cenocepacia J2315, an Epidemic Pathogen of Cystic Fibrosis Patients

et al. 2009

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“…Very little is known about the mechanism of resistance to APs in Burkholderia spp. LPS from various Burkholderia species, such as B. cepacia, B. caryophylli, and B. cenocepacia, contains Ara4N residues in the lipid A and also the unusual glycero-talo-octulosonic acid (Ko) residue in the inner-core oligosaccharide (10,13,19,20,25,26,31,32). Here, we show that a putative gene cluster for Ara4N biosynthesis and LPS modification is essential for the viability of B. cenocepacia.…”

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confidence: 94%

A Putative Gene Cluster for Aminoarabinose Biosynthesis Is Essential for Burkholderia cenocepacia Viability

Ortega¹,

et al. 2007

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Using a conditional mutagenesis strategy we demonstrate here that a gene cluster encoding putative aminoarabinose (Ara4N) biosynthesis enzymes is essential for the viability of Burkholderia cenocepacia. Loss of viability is associated with dramatic changes in bacterial cell morphology and ultrastructure, increased permeability to propidium iodide, and sensitivity to sodium dodecyl sulfate, suggesting a general cell envelope defect caused by the lack of Ara4N.

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“…Furthermore, modifications to the lipid A region can affect the overall charge of the LPS molecule. Burkholderia (Pseudomonas) cepacia is notoriously resistant to cationic antibacterial agents and has been found to have a very low number of phosphate groups and contains a 4-amino-arabinose sugar in place of a phosphate group in the lipid A molecule (2). Polymyxin-resistant mutants of E. coli K12 have been characterized and have been shown to contain increased amounts of PEtn in their lipid A molecules (15).…”

Section: Structural Characterization Of Lipid a Regions Of O-deacylatmentioning

confidence: 99%

Phosphorylation of the Lipid A Region of Meningococcal Lipopolysaccharide: Identification of a Family of Transferases That Add Phosphoethanolamine to Lipopolysaccharide

et al. 2003

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A gene, NMB1638, with homology to the recently characterized gene encoding a phosphoethanolamine transferase, lpt-3, has been identified from the Neisseria meningitidis genome sequence and was found to be present in all meningococcal strains examined. Homology comparison with other database sequences would suggest that NMB1638 and lpt-3 represent genes coding for members of a family of proteins of related function identified in a wide range of gram-negative species of bacteria. When grown and isolated under appropriate conditions, N. meningitidis elaborated lipopolysaccharide (LPS) containing a lipid A that was characteristically phosphorylated with multiple phosphate and phosphoethanolamine residues. In all meningococcal strains examined, each lipid A species contained the basal diphosphorylated species, wherein a phosphate group is attached to each glucosamine residue. Also elaborated within the population of LPS molecules are a variety of "phosphoforms" that contain either an additional phosphate residue, an additional phosphoethanolamine residue, additional phosphate and phosphoethanolamine residues, or an additional phosphate and two phosphoethanolamine residues in the lipid A. Mass spectroscopic analyses of LPS from three strains in which NMB1638 had been inactivated by a specific mutation indicated that there were no phosphoethanolamine residues included in the lipid A region of the LPS and that there was no further phosphorylation of lipid A beyond one additional phosphate species. We propose that NMB1638 encodes a phosphoethanolamine transferase specific for lipid A and propose naming the gene "lptA," for "LPS phosphoethenolamine transferase for lipid A."Lipopolysaccharide (LPS) is found in all gram-negative bacteria and is usually composed of three regions: lipid A, core oligosaccharide (OS), and a polysaccharide molecule often referred to as the "O-antigen." LPS from Neisseria meningitidis lacks the polysaccharide and is sometimes referred to as "lipooligosaccharide" (LOS) to reflect this. The core OS unit of N. meningitidis LPS comprises an inner core diheptose-N-acetylglucosamine backbone, wherein the two L-glycero-D-mannoheptose (Hep) residues can provide a point of attachment for outer core OS residues (8). Meningococcal LPS has been classified into 12 distinct LPS immunotypes (L1 to L12), originally defined by monoclonal antibody (MAb) reactivities (21) but further defined by structural analyses (4,5,7,9,14,16,26). The structural basis of the immunotyping scheme is primarily governed by the location of a phosphoethanolamine (PEtn) moiety on the distal heptose residue (HepII) at either the 3-or 6-position or absent, but is also dictated by the length and nature of OS extension from the proximal heptose residue (HepI) and the presence or absence of a glucose at HepII (17 [ Fig. 1]). The lipid A region of the LPS is responsible for much of the toxicity of the LPS molecule, and LPS is indeed sometimes referred to as "endotoxin." The lipid A region consists of a disaccharide of pyranosyl glucosamine r...

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Ionizing groups in lipopolysaccharides of Pseudomonas cepacia in relation to antibiotic resistance

Cited by 97 publications

References 42 publications

The Genome of Burkholderia cenocepacia J2315, an Epidemic Pathogen of Cystic Fibrosis Patients

The Genome of Burkholderia cenocepacia J2315, an Epidemic Pathogen of Cystic Fibrosis Patients

A Putative Gene Cluster for Aminoarabinose Biosynthesis Is Essential for Burkholderia cenocepacia Viability

Phosphorylation of the Lipid A Region of Meningococcal Lipopolysaccharide: Identification of a Family of Transferases That Add Phosphoethanolamine to Lipopolysaccharide

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