Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The percentage of beta-lactamase producing Haemophilus influenzae strains from patients with meningitis in The Netherlands increased from 0% in 1975/1976 to 4.6% in 1985/1986 (n = 1559). Twenty-three isolates resistant to ampicillin, penicillin, chloramphenicol, rifampicin and/or tetracycline were subtyped to determine if one resistant strain was spreading. (Sub)typing was performed by capsular typing, analysis of the major outer membrane protein patterns on sodium dodecylsulfate gels (SDS-PAGE subtypes), lipopolysaccharide serotyping and biotyping. The (sub)types of the resistant strains were similar to those of sensitive strains, thus indicating that antibiotic resistant strains develop at random.
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PMID:Comparison of antibiotic resistant and sensitive strains of Haemophilus influenzae type b in The Netherlands by outer-membrane protein subtyping. 313 38

Single doses of sodium ampicillin (10 mg/kg) and kanamycin sulfate (5 mg/kg) were administered intramuscularly (i.m.) separately, and then together, to five pony mares. The plasma antibiotic concentration-time curves were constructed. The pharmacokinetic parameters of the antibiotics given separately were not altered by concurrent administration. Four of the five pony mares were then given the i.m. kanamycin/ampicillin combination 4 h after acute synovitis and fever had been induced by injection of lipopolysaccharide into the left intercarpal joint. The plasma concentration-time curves and the synovial concentration-time curves of inflamed and normal joints were constructed. The Cmax of ampicillin in the lipopolysaccharide experiment was significantly higher than in the other experiments. The antibiotics entered the synovial fluid of the inflamed joints more quickly and attained higher concentrations than in the uninflamed joints. The ampicillin concentration exceeded 5 micrograms/ml in inflamed synovial fluid for some 2.5 h after injection, and kanamycin sulfate concentration exceeded 2 micrograms/ml for 7 h.
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PMID:Effect of induced synovial inflammation on pharmacokinetics and synovial concentration of sodium ampicillin and kanamycin sulfate after systemic administration in ponies. 328 68

A spontaneous one-step mutant of Salmonella paratyphi A selected on ampicillin showed cross-resistance to all beta-lactam antibiotics except imipenem and to aminoglycosides, chloramphenicol, tetracycline, trimethoprim, and quinolones. It also grew as small colonies. Examination of the cell envelope of the mutant showed a quantitative decrease in three major outer membrane proteins of 40.6, 39.6 (presumably porins), and 24 kilodaltons and quantitative as well as qualitative modifications in the ladder pattern of lipopolysaccharide. Direct evidence for decreased permeability in the mutant included reduced uptake of [3H]glucose and norfloxacin, reduced accessibility of aztreonam and benzylpenicillin to penicillin-binding proteins in whole cells, and decreased diffusion of lactose and cephaloridine into proteoliposomes that were reconstituted with outer membrane proteins from the mutant. There was also loss of invasiveness of the mutant into HeLa cells. We assume that a pleiotropic mutation was responsible for multiple alterations in the outer membrane components of the resistant mutant of S. paratyphi A.
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PMID:Mutation of Salmonella paratyphi A conferring cross-resistance to several groups of antibiotics by decreased permeability and loss of invasiveness. 336 43

In Escherichia coli K-12 the envA gene was previously shown to mediate chain formation and a decreased tolerance to several antibacterial agents. Phenethyl alcohol at low concentrations has now been found to increase the tolerance to actinomycin D, ampicillin, rifampin, and gentian violet in strains containing envA. The increased tolerance to gentian violet was correlated to a decreased uptake of the dye. A phenotype suppression of chain formation and colony morphology in envA mutants was also obtained. Except for an increase in palmitic acid, chemical analysis revealed no differences between an envA and its wild-type strain in the lipopolysaccharide part of the envelope. However, a decrease in the amount of phosphatidylglycerol and a C18: 1 fatty acid was observed in the extractable lipids of a strain containing envA. Growth in the presence of phenethyl alcohol reversed the changes in fatty acid and the phospholipid composition. Phenethyl alcohol was found to cause an immediate but transient inhibition of ribonucleic acid synthesis. It is suggested that this inhibition affects the penetrability barrier of the outer cell envelope layers in strains containing envA.
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PMID:Phenethyl alcohol as a suppressor of the envA phenotype associated with the envA gene in Escherichia coli K-12. 494 68

Class II ampicillin-resistant mutants of Escherichia coli are defined as having a twofold increase in penicillinase-mediated ampicillin resistance when determined by colony formation tests on plates. In this paper, one class II mutant has been compared to its parent strain. In liquid medium, the mutant was less resistant than the parent strain both in the absence and in the presence of R1 and R-factor mediating penicillinase activity. The penicillinase activity was found to be almost completely bound to the cells in the parent strain, whereas it was excreted to a great extent in the class II mutant strain. In liquid medium, resistance was well correlated to the cell-bound penicillinase activity, whereas the excreted penicillinases were also of great importance for survival on ampicillin plates. The mutant also had a changed resistance to a great number of other antibacterial drugs. The mutant was found to be more sensitive than the parent strain to osmotic shock, especially when treated with ethylenediaminetetraacetic acid or washed with sodium ions. However, the osmotic stability was restored by the presence of 1 mm Mg(2+) ions. The class II mutant was more sensitive than the parent strain to sodium cholate, and it adsorbed the phages T4 and T3-1 at a slower rate than did the parent strain. The two strains adsorbed T6 at the same rate. The class II phenotype could be gradually reversed by increasing concentrations of divalent cations. The pleiotropic changes in the phenotype are apparently unrelated to the specific targets for the antibacterial agents tested. They are secondary consequences of a cell envelope mutation. The findings indicate that the class II mutation mediates a structural change in the lipopolysaccharide of the cell envelope.
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PMID:Resistance of Escherichia coli to penicillins. 8. Physiology of a class II ampicillin-resistant mutant. 498 89

A mutant (G11el) of Escherichia coli selected as being resistant to ampicillin and showing signs of an envelope defect was also found to be tolerant to colicins E2 and E3. The colicin tolerance of G11el could be partially repressed by Mg(2+) ions. Transition from tolerance to sensitivity and vice versa by shifting the concentration of Mg(2+) in the growth medium required several generations. This indicated that synthesis of new envelope material was needed for transition. Previous physiological results have indicated a change in the envelope lipopolysaccharide (LPS) of G11el. However, chemical analyses revealed no differences in carbohydrate composition between LPS from G11el and its parent strain G11al. Genetic experiments showed that the mutation in G11el is located at about 20 min on the E. coli K-12 chromosome. The mutation was dominant over wild type in partial diploids with the mutation located on the episome. Because colicin tolerance was the most striking phenotypic effect as a result of mutation in the actual locus, this gene will be named tolD until the exact gene product is known. Spheroplasts formed from G11al and G11el by ethylenediaminetetraacetate-lysozyme treatment did not adsorb colicin E2; however, penicillin spheroplasts of G11al and G11el were tolerant to colicin E2. Thus, colicin tolerance can be induced biochemically. It is suggested that colicin tolerance often is a secondary consequence of a change in the cell envelope.
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PMID:Colicin tolerance induced by ampicillin or mutation to ampicillin resistance in a strain of Escherichia coli K-12. 499 99

The requirement for both plasmid and chromosomal genes in the biosynthesis of Shigella dysenteriae 1 lipopolysaccharide O antigen was demonstrated in Escherichia coli-Shigella hybrids. A 6-megadalton S. dysenteriae 1 plasmid, designated pWR23, was phenotypically tagged with the Tn3 ampicillin-resistance transposon. The tagged plasmid, designated pWR24, was transferred by transformation or conjugal mobilization to a rough E. coli K-12 recipient. Although the resultant hybrids were agglutinated in S. dysenteriae 1 antiserum, they did not remove all of the anti-Shiga agglutinins in absorption experiments. Modified lipid A core structure was detected in these hybrids, but Shiga O antigen was not expressed. When the his+ locus of the S. dysenteriae 1 chromosome was transferred by transduction to E. coli K-12 containing pWR24, complete Shiga O antigen was expressed. Lipopolysaccharide extracted from these hybrids was indistinguishable chemically, electrophoretically, and serologically from native S. dysenteriae 1 lipopolysaccharide.
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PMID:Expression of lipopolysaccharide O antigen in Escherichia coli K-12 hybrids containing plasmid and chromosomal genes from Shigella dysenteriae 1. 638 45

To determine whether the macrolide antibiotic erythromycin prevents microvascular leakage produced by lipopolysaccharide (LPS), we studied tracheae and lungs of pathogen-free rats. Tracheal vascular permeability and neutrophil recruitment were assessed by the percent area occupied by Monastral blue-labeled blood vessels and by myeloperoxidase-containing granulocytes, respectively, in tracheal whole mounts. Pulmonary microvascular leakage was evaluated by lung wet-to-dry (W/D) weight ratio. Inhalation of Escherichia coli LPS (5 mg/kg) caused time-dependent increases in tracheal vascular permeability, neutrophil influx, and lung W/D ratio. These responses were inhibited by pretreatment with oral erythromycin, but not by ampicillin or cefaclor, in a dose-dependent manner: erythromycin at 10 mg/kg daily for 1 wk reduced the area density of Monastral blue-labeled vessels from 6.7 +/- 1.2 to 1.4 +/- 0.3% (p < 0.01), the number of neutrophils (from 365 +/- 51 to 149 +/- 30 cells/mm2, p < 0.01), and lung W/D weight ratio (from 6.76 +/- 0.30 to 5.39 +/- 0.21, p < 0.01). This inhibitory effect of erythromycin was abolished by depletion of circulating neutrophils with cyclophosphamide. These results suggest that LPS causes acute lung injury, microvascular leakage, and neutrophil recruitment in the trachea, and that erythromycin protects against these changes, probably by acting on neutrophils.
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PMID:Effect of erythromycin on endotoxin-induced microvascular leakage in the rat trachea and lungs. 773 18

In Nicaragua, in 1989, health workers obtained urethral or cervical samples from 18 people with gonorrhea attending public health clinics in Managua and sent them to the National Laboratory of Public Health in Managua for characterization of their antibiotic susceptibility. Of the 18 strains, 15 (83.3%) were of the auxotype/serotype Proto/PIB. Electrophoresis of lipopolysaccharides on SDS-polyacrylamide gels (15%) with 4 M urea revealed no difference in lipopolysaccharide profiles for all strains. The variable expression of the 31-kDa opacity outer membrane protein was not related to antimicrobial resistance. All isolates exhibited susceptibility to ceftriaxone, spectinomycin, cefazolin, cefoxitin, and rifampin. 78% of the strains produced beta-lactamase. 89% of the strains were resistant to penicillin and ampicillin, 44% were resistant to tetracycline, 28% were resistant to cefamandol, 22% were resistant to chloramphenicol, and 11% were resistant to erythromycin. There were 5 distinct groups of Neisseria gonorrhoeae isolated according to their plasmid profiles. The largest was plasmid profile group 1 (55.6%), defined as carrying the 24.5, 3.2, and 2.6 MDa plasmids. It produced beta-lactamase. Penicillinase-producing N. gonorrhoeae (PPNG) comprised 78% of the isolates, 22% of whom were tetracycline-resistant N. gonorrhoea. One PPNG strain exhibited a parallel decrease of penicillin binding to penicillin-binding protein 2. These findings confirmed the presence of multiresistant N. gonorrhoeae strains in Managua, Nicaragua. Based on these findings, the researchers recommended that penicillin and tetracycline not be used to treat gonorrhea in Nicaragua; they recommended ceftriaxone and spectinomycin.
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PMID:Characterization of multiresistant strains of Neisseria gonorrhoeae isolated in Nicaragua. 810 53

Two broadly cross-reactive anti-lipopolysaccharide core monoclonal antibodies WN1 222.5 and SZ27/150.3 were used in an ELISA system to detect the accessibility of core epitopes in Escherichia coli (four clinical isolates and NCTC 10418) grown to early stationary phase in the absence and presence of a half, a quarter and an eighth the MIC of temocillin, ampicillin, chloramphenicol, gentamicin and ciprofloxacin. The bacteria were coated on to ELISA microtitre plates. By comparing ELISA-titre ratios, temocillin induced a significantly large increase in binding of WN1 222.5 to all strains except NCTC 10418. Ampicillin and chloramphenicol induced a small increase in the binding of WN1 222.5 in some instances. Ciprofloxacin and gentamicin caused no increase in binding. Lipopolysaccharide SZ27/150.3 was only tested against temocillin-grown bacteria, but binding was not increased significantly compared with WN1 222.5. The results obtained demonstrate the potential use of temocillin to improve the clinical efficacy of immunotherapeutic monoclonal antibodies in Gram-negative sepsis.
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PMID:The accessibility of cross-reactive anti-lipopolysaccharide-core monoclonal antibodies to Escherichia coli grown in sub-MICs of temocillin and other antibiotics. 833 96


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