Smith-degradative studies on the polysaccharide portion of A-band lipopolysaccharide from a mutant (AK1401) of Pseudomonas aeruginosa strain PAO1

1994 ◽  
Vol 72 (5) ◽  
pp. 1376-1382 ◽  
Author(s):  
Todd L. Arsenault ◽  
David B. MacLean ◽  
Wei Zou ◽  
Walter A. Szarek
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mass Spectrometric ◽  
Minor Components ◽  
Strain Pao1 ◽  
Smith Degradation ◽  
Mass Spectrometric Evidence

Hepta-O-acetyl-O-α-D-Rhap-(1 → 3)-O-α-D-Rhap-(1 → 2)-glycerol (5) was the major component derived by way of Smith degradation of A-band polysaccharide (a D-rhamnan isolated from a mutant, AK1401, of Pseudomonas aeruginosa strain PAO1). The structure has been verified by an unambiguous synthesis of 5. Based on mass spectrometric evidence, hepta-O-acetyl-O-Ribp-(1 → 3)-O-α-D-Rhap-(1 → 2)-glycerol is considered to be one of the minor components. The Smith degradation of A-band polysaccharide and the synthesis of 5 are reported.

scholarly journals Composition of Pseudomonas aeruginosa slime

1969 ◽  
Vol 112 (4) ◽  
pp. 521-525 ◽  
Author(s):  
M. R. W. Brown ◽  
J. H. Scott Foster ◽  
J. R. Clamp
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Hyaluronic Acid ◽  
Nucleic Acid ◽  
Growth Medium ◽  
Extraction Procedure ◽  
The Other ◽  
Minor Components ◽  
Polysaccharide Fraction ◽  
Defined Media ◽  
Rna And Dna

1. The slime produced by eight strains of Pseudomonas aeruginosa on a number of different media was demonstrated to be qualitatively the same. Small quantitative differences may be occasioned by differences in the extraction procedure, the growth medium or the strain of organism used. 2. The slime was shown to be predominantly polysaccharide with some nucleic acid material and a small amount of protein. 3. The hydrolysed polysaccharide fraction consists mainly of glucose with smaller amounts of mannose. This accounts for some 50–60% of the total slime. In addition, there is some 5% of hyaluronic acid. The nucleic acid material represents approx. 20% of the total weight, and is composed of both RNA and DNA. 4. Minor components are protein, rhamnose and glucosamine, the protein being less than 5% of the total. 5. Hyaluronic acid is produced in greater quantities from nutrient broth than from chemically defined media, and is more firmly attached to the cells than the other components.

scholarly journals Pseudomonas aeruginosa las and rhl quorum-sensing systems are important for infection and inflammation in a rat prostatitis model

Microbiology ◽  
2009 ◽  
Vol 155 (8) ◽  
pp. 2612-2619 ◽  
Author(s):  
Lisa K. Nelson ◽  
Genevieve H. D'Amours ◽  
Kimberley M. Sproule-Willoughby ◽  
Douglas W. Morck ◽  
Howard Ceri
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Tissue Damage ◽  
Inflammatory Markers ◽  
Bacterial Colonization ◽  
Opportunistic Pathogen ◽  
Infection Model ◽  
Chronic Infections ◽  
Strain Pao1 ◽  
Rat Prostate

Pseudomonas aeruginosa frequently acts as an opportunistic pathogen of mucosal surfaces; yet, despite causing aggressive prostatitis in some men, its role as a pathogen in the prostate has not been investigated. Consequently, we developed a Ps. aeruginosa infection model in the rat prostate by instilling wild-type (WT) Ps. aeruginosa strain PAO1 into the rat prostate. It was found that Ps. aeruginosa produced acute and chronic infections in this mucosal tissue as determined by bacterial colonization, gross morphology, tissue damage and inflammatory markers. WT strain PAO1 and its isogenic mutant PAO-JP2, in which both the lasI and rhlI quorum-sensing signal systems have been silenced, were compared during both acute and chronic prostate infections. In acute infections, bacterial numbers and inflammatory markers were comparable between WT PA01 and PAO-JP2; however, considerably less tissue damage occurred in infections with PAO-JP2. Chronic infections with PAO-JP2 resulted in reduced bacterial colonization, tissue damage and inflammation as compared to WT PAO1 infections. Therefore, the quorum-sensing lasI and rhlI genes in Ps. aeruginosa affect acute prostate infections, but play a considerably more important role in maintaining chronic infections. We have thus developed a highly reproducible model for the study of Ps. aeruginosa virulence in the prostate.

scholarly journals A Rapid Phenotypic Whole-Cell Screening Approach for the Identification of Small-Molecule Inhibitors That Counter β-Lactamase Resistance in Pseudomonas aeruginosa

2017 ◽  
Vol 23 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Deanna Collia ◽  
Thomas D. Bannister ◽  
Hao Tan ◽  
Shouguang Jin ◽  
Taimour Langaee ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Small Molecule ◽  
Small Molecule Inhibitors ◽  
Laboratory Strain ◽  
Multidrug Resistant ◽  
First Line ◽  
Strain Pao1 ◽  
Whole Cell ◽  
Bacterial Sensitivity ◽  
Opportunistic Human Pathogen

Pseudomonas aeruginosa is an opportunistic human pathogen that is prevalent in hospitals and continues to develop resistance to multiple classes of antibiotics. Historically, β-lactam antibiotics have been the first line of therapeutic defense. However, the emergence of multidrug-resistant (MDR) strains of P. aeruginosa, such as AmpC β-lactamase overproducing mutants, limits the effectiveness of current antibiotics. Among AmpC hyperproducing clinical isolates, inactivation of AmpG, which is essential for the expression of AmpC, increases bacterial sensitivity to β-lactam antibiotics. We hypothesize that inhibition of AmpG activity will enhance the efficacy of β-lactams against P. aeruginosa. Here, using a highly drug-resistant AmpC-inducible laboratory strain PAO1, we describe an ultra-high-throughput whole-cell turbidity assay designed to identify small-molecule inhibitors of the AmpG. We screened 645,000 compounds to identify compounds with the ability to inhibit bacterial growth in the presence of cefoxitin, an AmpC inducer, and identified 2663 inhibitors that were also tested in the absence of cefoxitin to determine AmpG specificity. The Z′ and signal-to-background ratio were robust at 0.87 ± 0.05 and 2.2 ± 0.2, respectively. Through a series of secondary and tertiary studies, including a novel luciferase-based counterscreen, we ultimately identified eight potential AmpG-specific inhibitors.

Gas chromatographic/mass spectrometric evidence for the identification of 6,7-dihydroxy-1, 2,3,4-tetrahydroisoquinoline as a normal constituent of rat brain

1981 ◽  
Vol 30 (17) ◽  
pp. 2461-2468 ◽  
Author(s):  
Steven A. Barker ◽  
John A. Monti ◽  
Lelland C. Tolbert ◽  
George B. Brown ◽  
Samuel T. Christian
Keyword(s):  
Rat Brain ◽  
Mass Spectrometric ◽  
Mass Spectrometric Evidence ◽  
Normal Constituent ◽  
Chromatographic Mass

scholarly journals The Pseudomonas aeruginosa Sensor Kinase KinB Negatively Controls Alginate Production through AlgW-Dependent MucA Proteolysis

2009 ◽  
Vol 191 (7) ◽  
pp. 2285-2295 ◽  
Author(s):  
F. Heath Damron ◽  
Dongru Qiu ◽  
Hongwei D. Yu
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Response Regulator ◽  
Negative Regulator ◽  
Loss Of Function ◽  
Cystic Fibrosis Mutation ◽  
Strain Pao1 ◽  
Alginate Production ◽  
Mucoid Conversion ◽  
Σ Factor ◽  
Lung Infections

ABSTRACT Mucoidy, or overproduction of the exopolysaccharide known as alginate, in Pseudomonas aeruginosa is a poor prognosticator for lung infections in cystic fibrosis. Mutation of the anti-σ factor MucA is a well-accepted mechanism for mucoid conversion. However, certain clinical mucoid strains of P. aeruginosa have a wild-type (wt) mucA. Here, we describe a loss-of-function mutation in kinB that causes overproduction of alginate in the wt mucA strain PAO1. KinB is the cognate histidine kinase for the transcriptional activator AlgB. Increased alginate production due to inactivation of kinB was correlated with high expression at the alginate-related promoters P algU and P algD . Deletion of alternative σ factor RpoN (σ54) or the response regulator AlgB in kinB mutants decreased alginate production to wt nonmucoid levels. Mucoidy was restored in the kinB algB double mutant by expression of wt AlgB or phosphorylation-defective AlgB.D59N, indicating that phosphorylation of AlgB was not required for alginate overproduction when kinB was inactivated. The inactivation of the DegS-like protease AlgW in the kinB mutant caused loss of alginate production and an accumulation of the hemagglutinin (HA)-tagged MucA. Furthermore, we observed that the kinB mutation increased the rate of HA-MucA degradation. Our results also indicate that AlgW-mediated MucA degradation required algB and rpoN in the kinB mutant. Collectively, these studies indicate that KinB is a negative regulator of alginate production in wt mucA strain PAO1.

Human Prestin: A Candidate PE1 Protein Lacking Stringent Mass Spectrometric Evidence?

2017 ◽  
Vol 16 (12) ◽  
pp. 4531-4535 ◽  
Author(s):  
Abidali Mohamedali ◽  
Seong Beom Ahn ◽  
Varun K. A. Sreenivasan ◽  
Shoba Ranganathan ◽  
Mark S. Baker
Keyword(s):  
Mass Spectrometric ◽  
Mass Spectrometric Evidence
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