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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

R-plasmid RP1 was transferred to Pseudomonas aeruginosa cells, as indicated by their resistance to carbenicillin, ampicillin, cephaloridine, kanamycin, and tetracycline, and by the presence of a periplasmic beta-lactamase. The wild-type cells (RP1-) were lysed by ethylenediaminetetraacetic acid but not by ethylene-glycol-bis(2-aminoethyl ether)-N,N-tetraacetic acid, whereas cells carrying the plasmid (RP1+) were resistant to both these chelating agents. RP1+ and RP1- strains were both sensitive to the lytic action of polymyxin B and the lethal action of cold shock, but the effect was less marked in the RP1+ cultures. A proportion of the RP1+ cells surviving cold shock lost resistance to carbenicillin, tetracycline, and kanamycin. The chemical composition of whole cells and cell walls of RP1+ differed from that RP1- in the content of cation, phospholipid, and markers for lipopolysaccharide and peptidoglycan. Differences in cell wall composition, response to ethylenediaminetetraacetic acid and polymyxin B, and the effects of cold shock are all compatible with the hypothesis that RP1 confers changes in the cell envelope, probably in the outer membrane, of P. aeruginosa.
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PMID:Influence of R-plasmid RP1 of Pseudomonas aeruginosa on cell wall composition, drug resistance, and sensitivity to cold shock. 12 23

Lipopolysaccharide-defective mutants of Pseudomonas aeruginosa strain PAO have been isolated on the basis of their resistance to lipopolysaccharide-specific bacteriophages. These mutants have been differentiated by their agglutination in NaCl and acriflavine, phage sensitivity, and chemical analysis of the lipopolysaccharides. The susceptibility of the wild-type strain and four mutants to a series of twenty-six agents, including dyes, detergents, antibiotics, and lysozyme, was examined. The roughest mutant (AK-43) exhibited increased susceptibility to sodium deoxycholate, hexadecylpyridinium chloride, benzalkonium chloride, ampicillin, penicillin G, erythromycin, colymycin, and polymyxin B. The role of cell envelope fractions in antibiotic resistance in P. aeruginosa is discussed.
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PMID:Susceptibility of lipopolysaccharide-defective mutants of Pseudomonas aeruginosa strain PAO to dyes, detergents, and antibiotics. 12 25

Mutants of Escherichia coli K12, defective in phosphatidylserine synthetase (pss), can be isolated as temperature-sensitive, conditional lethals. When cultivated at intermediate temperatures (30 degrees), such mutants contain approximately 3 times more phosphatidylglycerol plus cardiolipin (and less phosphatidylethanolamine) than normal. We now wish to report that, under these conditions, the pss-8 mutant is hypersensitive to certain antibiotics, especially to streptomycin, kanamycin, and gentamicin, although also to ampicillin and novobiocin. At 30 degrees, the membrane protein and fatty acid composition of pss-8 is nearly normal, i.e. identical with an isogenic pss+ organism. Radiochemical labeling and bacteriophage growth studies show that lipopolysaccharide is also unaltered. Therefore, the antibiotic hypersensitivity of pss-8 differs from previously reported hypersensitivities, associated with lipopolysaccharide defects. These results suggest that the polar phospholipid headgroups may play an important role in maintaining the barrier function of the outer gramnegative membrane and that putative inhibitors of the phosphatidylserine synthetase might potentiate the action of numerous antibiotics currently in clinical use.
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PMID:Envelope composition and antibiotic hypersensitivity of Escherichia coli mutants defective in phosphatidylserine synthetase. 19 63

The lipopolysaccharides of ampicillin-resistant cell-wall-defective mutants of Escherichia coli K-12 were analyzed. From their lipopolysaccharides the respective core oligosaccharides were obtained. Following dephosphorylation,the core oligosaccharides were methylated and analyzed by gas chromatography/mass spectrometry. From core-defective mutants substructures of the K-12 core were obtained. Analysis of the lipopolysaccharide preparations from wild-type K-12 indicated the presence of several core structures with different degrees of completion. The lipopolysaccharide preparation was degraded and the oligosaccharide mixture was partially resolved by gel filtration chromatography. Methylation, gas chromatography and mass spectrometry of the oligosaccharides permitted the tentative formulation of the K-12 core structure. Alternative interpretations for this heterogeneity are discussed.
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PMID:Cell-wall lipopolysaccharides of ampicillin-resistant mutants of Escherichia coli K-12. 78 Jan 12

A study recently conducted across Canada showed that 64 of 2,503 clinical isolates of Haemophilus influenzae were resistant to beta-lactams without production of a beta-lactamase (L. D. Tremblay, J. L'Ecuyer, P. Provencher, M. G. Bergeron, and Canadian Study Group, Can. Med. Assoc. J. 143:895-900, 1990). The beta-lactamase-negative strains formed three distinct groups, with ampicillin MICs of 0.5 to 1, 2 to 4, and greater than or equal to 8 micrograms/ml for groups I, II, and III, respectively. We have investigated the mechanisms of resistance for eight strains originating from different infections and geographic areas. These strains were representative of groups I to III. Five strains were nontypeable, two were type B, and one was non-B. Chromosomal DNA extracted from each strain was used to transform the laboratory strain Rd. Transformants were selected on beta-lactam-containing plates and showed the same level of resistance to ampicillin as the donor strains. Differences in outer membrane proteins, porins, and lipopolysaccharide profiles on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) did not change with resistance. Functional analyses of purified porins in artificial lipid bilayer experiments did not explain resistance. Peptidoglycan synthesis was measured by incorporation of [14C]alanine into trichloroacetic acid-insoluble cell wall material in the presence of chloramphenicol. The growth rate and the rate of peptidoglycan synthesis observed for the transformants of the isogenic set did not correlate with resistance. Whole-cell labeling with 125I-penicillin revealed modifications in penicillin-binding proteins (PBPs) among the transformants. In particular, PBPs 3A and 3B (65 and 63 kDa, respectively) showed a decrease in affinity for beta-lactams in all transformants (groups I, II, and III) and correlated with an increased MIC except in the transformant of group III, which showed higher levels of resistance. Partial purification and proteolytic digestion of 125I-penicillin-labeled PBP 3B led to two types of CnBr peptide profiles on SDS-PAGE, the profiles of the transformed strains from groups I and II being different from those of the control group and group III. Finally, electron microscopy revealed a distinct cell filamentation for the group III transformants. These data clearly indicate that changes in PBPs are a common mechanism that results in a significant level of non-beta-lactamase-mediated beta-lactam resistance in H. influenzae despite serotype, origin of isolation, or geographic distribution.
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PMID:Molecular basis of the non-beta-lactamase-mediated resistance to beta-lactam antibiotics in strains of Haemophilus influenzae isolated in Canada. 151 Apr 47

Resistant variants of three clinical Pseudomonas aeruginosa isolates were obtained in the presence of aztreonam. The variants exhibited a four- to eightfold increase in the minimal inhibitory concentrations to beta-lactam antibiotics (except imipenem) to quinolones, such as norfloxacin and fleroxacin, chloramphenicol and tetracycline, but not to gentamicin and polymyxin B. beta-Lactamase production was barely detectable in both wild-type strains and the resistant clones. Only ampicillin, cefoxitin and imipenem increased the production of beta-lactamase, whereas various other beta-lactams did not. Penicillin-binding proteins remained unchanged in the aztreonam-resistant clones. The analysis of the outer membrane proteins did not reveal differences in the outer membrane proteins between the wild-type strains and the aztreonam-resistant clones. Two of the three antibiotic-resistant isogenic clones contained less lipopolysaccharides (LPSs) than their corresponding wild-type strains. Moreover, it could be demonstrated that the ratio of 2-keto-3-deoxy octonate to carbohydrate of the LPS changed in any case between the wild-type strains and the aztreonam-resistant clones. These alterations were accompanied by a decrease in surface hydrophobicity of the resistant clones as compared to the wild-type strains. Therefore, quantitative as well as qualitative alterations in the LPS may provide an explanation for the resistant phenotype observed.
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PMID:Lipopolysaccharide alterations responsible for combined quinolone and beta-lactam resistance in Pseudomonas aeruginosa. 159 50

During six days in November, 1987, 611 pupils (age range 7-19 years) and 39 adults (23-57) at a school complex in southern Finland had diarrhoea due to Escherichia coli O111:B4. Diarrhoea developed in 137 other household members during the two weeks after the school outbreak. The source of the organism remains unknown. The outbreak strains, when incubated at 22 degrees C or exposed to ampicillin, lost the lipopolysaccharide O antigen and began to react with antisera against Salmonella typhi Vi antigen. The Vi antigen-like reactivity increased the adherence of the organisms to Hep-2 cells. These results indicate that E coli O111:B4, and possibly other enteropathogenic E coli strains, should be considered in the diagnosis of all diarrhoea cases and not only in infantile diarrhoea. Expression of Vi antigen in E coli may play a part in virulence by enhancing adherence to the intestinal epithelium.
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PMID:Outbreak of diarrhoea due to Escherichia coli O111:B4 in schoolchildren and adults: association of Vi antigen-like reactivity. 197 76

Outbreaks of Shigella dysenteriae I occurred in northeastern Thailand in the fall of 1986 and again in the spring and fall of 1987 for the first time in over 20 years. The epidemic strain of S. dysenteriae I was resistant to tetracycline, streptomycin, chloramphenicol, and trimethoprim-sulfamethoxazole, but susceptible to ampicillin. Trimethoprim resistance was chromosomally encoded by type I dihydrofolate reductase. In Ubon Province, where 10,000 cases of dysentery were reported, there were 3-5 cases of dysentery per 1,000 residents during the peak months, with 2-5 hospitalizations per 100 cases of reported dysentery. There were 2 deaths among 101 hospitalized, culture-confirmed cases. The overall case-fatality rate among reported cases of dysentery in this province was 0.9%. In contrast to S. flexneri infections, which occurred predominantly among children less than 5 years old, S. dysenteriae I infections occurred in all age groups. The large number of susceptibles appeared to be important in allowing rapid spread of S. dysenteriae I. In 1 village, 46% of 434 villagers reported dysentery; S. dysenteriae I was isolated from 24 out of 81 (30%) individuals cultured. Based on the prevalence of IgG antibody to S. dysenteriae I lipopolysaccharide, it was estimated that 76% of the villagers had been infected.
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PMID:Introduction and spread of multi-resistant Shigella dysenteriae I in Thailand. 264 59

Far-ultraviolet radiation (254 nm) at a dose of 10, 20, and 30 J/m2 was found to disrupt the outer membrane permeability barrier of Escherichia coli to various antibiotics, dyes, and detergents. The degree of sensitization to these agents was proportional to the radiation dose. The irradiated cells showed a significant increase in the sensitivity of hydrophilic antibiotics (ampicillin, carbenicillin, penicillin), whereas much less sensitization was found towards hydrophobic probes (kanamycin, erythromycin, rifamycin SV, crystal violet, phenol, novobiocin) and detergents (dodecyl sulfate, bile salt, Triton X-100). The biochemical data and ultrastructural analysis of the outer membrane by freeze-etching have shown that the increase in phospholipid:protein ratio after irradiation had changed the architecture of the outer membrane from a highly asymmetric bilayer structure with densely packed lipopolysaccharide--protein particles on the outer half, to one predominantly exhibiting smooth phospholipid bilayer characteristics. The structure, composition, and barrier function of the outer membrane were restored to normal within 3 h of postirradiation incubation in nonproliferative medium. During this period, the acquisition of resistance towards a hydrophilic antibiotic (ampicillin) was faster than that for a hydrophobic agent (phenol).
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PMID:Influence of far-ultraviolet radiation on the permeability of the outer membrane of Escherichia coli. 269 96

The mechanism of Pseudomonas aeruginosa resistance to imipenem in five imipenem-susceptible clinical isolates and in their resistant counterparts was investigated. The frequency for selecting imipenem-resistant variants ranged from 2.7 X 10(-5) to 2.1 X 10(-8) and was comparable to those for other beta-lactams. Cross-resistance between imipenem and other beta-lactam compounds was not observed. In all imipenem-resistant variants, induction of chromosomal beta-lactamase by imipenem was markedly diminished compared with that in the susceptible parent strain. This was not the case for other inducers such as ampicillin or cefoxitin, suggesting an impaired uptake of imipenem as an explanation for resistance. Analysis of the outer membrane proteins revealed a marked decrease of either a 46- or a 45-kilodalton protein. The lipopolysaccharide of the outer membrane in the imipenem-resistant variants was not altered.
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PMID:Imipenem resistance in Pseudomonas aeruginosa resulting from diminished expression of an outer membrane protein. 311 61


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