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)

Rat urine was found to contain a component showing cross-reactivity with antibody against rat plasma angiotensinogen. Sodium dodecyl sulfate polyacrylamide gel electrophoresis of rat urine revealed antigenic bands corresponding to the molecular weights of plasma angiotensinogen. The urinary angiotensinogen excretion in 8 rats, determined by direct radioimmunoassay, was 2.70 +/- 0.21 micrograms/day. Induction of acute inflammation in rats by injection of lipopolysaccharide caused about a 7-fold increase of urinary angiotensinogen excretion in the 24 hr after injection, with a concomitant elevation of plasma angiotensinogen. Neither sodium depletion nor loading by a low- or high-sodium diet altered the urinary excretion of angiotensinogen. These results suggest that the angiotensinogen present in rat urine is derived from that in plasma, although the level of excretion is too low to have any influence on the plasma level of angiotensinogen.
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PMID:Angiotensinogen excretion in rat urine: effects of lipopolysaccharide treatment and sodium balance. 180 Jul 98

The adherence of lipopolysaccharides (LPSs) from periodontal disease-associated bacteria to saliva-coated hydroxyapatite (S-HA) and serum-coated HA beads was examined by chromogenic Limulus activity (toxicolor test). Phenol-water extracted LPS preparations from Bacteroides intermedius, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, Eikenella corrodens, and rough-type LPS from Escherichia coli adhered to S-HA and serum-coated beads and agglutinated human erythrocytes. The adhered LPSs to S-HA and serum-coated HA beads were not removed by vigorous washing with distilled water. LPSs from Bacteroides (Porphyromonas) gingivalis strains and wild-type E. coli did not adhere to S-HA, serum-coated HA beads or show hemagglutinating activity. SDS-PAGE patterns stained with silver stain showed that LPSs adhered to S-HA, and serum-coated HA beads and erythrocytes possessed a distinct fast-migrating band similar to rough-type LPS. B. gingivalis LPSs possessed slow-migrating and repeating ladder bands similar to wild-type LPS.
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PMID:Adherence to experimental pellicle of rough-type lipopolysaccharides from subgingival plaque bacteria. 181 66

Laminin receptor was isolated from gastric epithelial cell membrane by the procedure involving membrane solubilization with octylglucoside followed by affinity chromatography on laminin-coupled Sepharose. The receptor protein, eluted from the matrix with cation-free EDTA buffer, yielded on SDS-PAGE a single 67kDa band. After radioiodination, the protein was incorporated into liposomes which displayed specific affinity toward the laminin-coated surface. The binding of liposomal receptor to the laminin-coated surface was inhibited by lipopolysaccharide from H.pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 50 micrograms/ml at which point a 96% decrease in the receptor binding occurred. It is suggested that a similar process may account for the loss of mucosal integrity in the pathogenesis of H. pylori associated gastric disease.
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PMID:Inhibition of gastric mucosal laminin receptor by Helicobacter pylori lipopolysaccharide. 182 58

The maintenance of gastric mucosal integrity depends upon the interaction involving specific cell surface receptors with distinct proteins of extracellular matrix, one of which is laminin. We present here evidence that lipopolysaccharide from Helicobacter pylori interferes with laminin binding on the receptor. The laminin receptor was isolated from gastric epithelial cell membrane by the procedure involving membrane solubilization with octylglucoside followed by affinity chromatography on laminin-coupled Sepharose. The receptor protein yielded on SDS-PAGE a single 67 kDa band. After radioiodination, the protein was incorporated into liposomes which displayed specific affinity toward laminin-coated surface. The binding of liposomal receptor to the laminin-coated surface was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 50 micrograms/ml, at which a 96% decrease in binding occurred. Introduction of sucralfate to the assay system led to the prevention of the inhibitory effect of lipopolysaccharide on the receptor-laminin binding. The effect was dose dependent and, at sucralfate concentration of 45 micrograms/ml, nearly complete restoration in binding was achieved. The results suggest that H. pylori also may be capable of disrupting the gastric mucosal integrity through a similar mechanism in vivo, and that anti-ulcer drug sucralfate counteracts this effect.
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PMID:Inhibition of gastric mucosal laminin receptor by Helicobacter pylori lipopolysaccharide: effect of sucralfate. 183 19

A laminin receptor was isolated from bovine gingival epithelial-cell membrane. After solubilization with octylglucoside, the receptor was subjected to affinity chromatography on laminin-coupled Sepharose and eluted with cation-free EDTA buffer yielding on SDS-PAGE a 67 kDa protein band. After radioiodination, the protein was incorporated into liposomes which displayed specific affinity towards laminin-coated surfaces, as well as to tooth cementum. The binding of receptor protein to cementum was inhibited by lipopolysaccharide from Bacteroides gingivalis. Preincubation of cementum with the lipopolysaccharide decreased the binding of the liposomal laminin-receptor preparation by 35.8%, while a 59.2% decrease in binding occurred when the lipopolysaccharide was preincubated with the receptor, suggesting that the lipopolysaccharide interfered with the laminin binding site on the receptor. The results demonstrate the existence of a specific gingival cell-surface laminin receptor, show that it is capable of binding to cementum, and provide evidence for the disruption of this process by bacterial lipopolysaccharide. This mechanism may account for the loss of gingival attachment in the pathogenesis of periodontal disease.
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PMID:Inhibition of bovine gingival laminin receptor by bacterial lipopolysaccharide. 187 30

Monoclonal antibodies (MAbs) were raised against the major, 46-48-Kda outer-membrane proteins of Vibrio cholerae O1. The hybridoma clones were screened by enzyme-linked immunosorbent assay (ELISA) with cell-surface proteins of V. cholerae O1 as the coating antigen. Four hybridomas, which secreted anti-V. cholerae cell-surface-protein antibodies, were subcloned by limiting dilution and obtained as ascites in vivo. A MAb of the IgG1 subclass was isolated in good yield from the murine ascites by affinity chromatography with recombinant protein G-Sepharose 4B. It gave positive reactions, as determined by ELISA, against cell-surface proteins prepared from both biotypes (classical and El Tor) and both serotypes (Ogawa and Inaba) of V. cholerae O1. The MAb did not have any reactivity towards V. cholerae lipopolysaccharide preparations. Immunoblotting studies were performed on cell-surface proteins separated by one-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis (1D SDS-PAGE) and also by two-dimensional (2D) electrophoresis with iso-electric focusing in the first dimension followed by SDS-PAGE in the second dimension. When proteins were separated by 1D SDS-PAGE, only one band at 46-48 Kda reacted with the MAb. This protein appeared to consist of two narrowly-spaced and cross-reactive bands when a nitrocellulose blot, obtained by 2D SDS-PAGE, was exposed to the MAb.
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PMID:Production and characterisation of monoclonal antibodies to outer-membrane-protein antigens of Vibrio cholerae O1. 190 61

A rifampin-resistant mutant of Brucella abortus, designated RB51, was derived by repeated passage of strain 2308 on Trypticase soy supplemented with 1.5% agar and varying concentrations rifampin or penicillin. The RB51 colonies absorbed crystal violet and RB51 cell suspensions autoagglutinated, indicating a rough type colonial morphology for this strain. No O-chain component was detected in lipopolysaccharide (LPS) extracted from RB51 on SDS-PAGE gels stained with silver. Western blot analysis with the monoclonal antibody BRU 38, which is specific for the perosamine homopolymer O-chain of smooth Brucella LPS, indicated that the LPS of RB51 is highly deficient in O-chain when compared with the parenteral smooth strain 2308 or rough strain 45/20. Biochemically, RB51 resembles parental strain 2308 in its ability to utilize erythritol. Intraperitoneal inoculation of RB51 into mice results in a splenic colonization which is cleared within four weeks post infection. RB51 does not revert to smooth colony morphology upon passage in vivo (mice) or in vitro. Mice infected with RB51 produce antibodies against B. abortus antigens including class 2 and 3 outer membrane proteins but not against the O-chain. Furthermore, rabbits, goats and cattle hyperimmunized with sonicates of RB51 develop antibodies to B. abortus cellular antigens but do not develop antibodies specific for the O-chain. Immunization of mice with 1 x 10(8) viable RB51 organisms confers significant protection against challenge with virulent B. abortus strain 2308.
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PMID:Biological properties of RB51; a stable rough strain of Brucella abortus. 190 58

Lipase was isolated from P. aeruginosa by ultrafiltration of sterile-filtered culture supernatant. Gel filtration on Sepharose 4B yielded a broad peak corresponding to a molecular mass range of 100 to 1000 kDa. Electron microscopy of a negatively stained lipase preparation after Sepharose 4B chromatography revealed spherical particles with diameters ranging from 5 to 20 nm. Biochemical characterization and SDS polyacrylamide gel electrophoresis suggested that these particles consisted of protein and carbohydrate including lipopolysaccharide with the major enzyme activity being lipase. Various concentrations of this lipase preparation were preincubated with human peripheral blood neutrophils and monocytes. The chemotaxis and chemiluminescence of these cells were then determined. It was shown that lipase inhibited the monocyte chemotaxis and chemiluminescence, whereas it had no or very little effect on neutrophils. The inhibitory effect was concentration dependent and was abolished by heat treatment of the enzyme at 100 degrees C. Since monocytes are one of the important cells of the host defence system the inhibition of the function of these cells may contribute to the pathogenesis of infections caused by P. aeruginosa.
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PMID:Extracellular lipase of Pseudomonas aeruginosa: biochemical characterization and effect on human neutrophil and monocyte function in vitro. 191 Jan 41

The lipopolysaccharides of Actinobacillus actinomycetemcomitans strain Y4 and a human clinical isolate PO 1021-7 were examined by SDS/PAGE, deoxycholate/PAGE and mass spectrometry. PAGE analysis revealed an electrophoretic pattern similar to the SR-type lipopolysaccharide (LPS) of Salmonella. Deoxycholate/PAGE indicated the LPS of A. actinomycetemcomitans to consist of short sugar chains. Chemical analysis revealed the presence of thiobarbituric-acid-positive material (3-deoxy-D-manno-octulosonic acid equivalents) and four neutral sugars: glucose, galactose, D-glycero-D-manno-heptose and L-glycero-D-manno-heptose. Phosphate, glucosamine, glycine, and the fatty acids, 3-hydroxymyristic acid, myristic acid and palmitic acid, comprised the remainder of the molecule. The structure of the free lipid A revealed it to consist of a 1,6-glucosamine disaccharide esterified at C4' by a phosphomonoester. The hydroxyl group at C3 and the amide group of the non-reducing glucosamine were both acylated by 3-myristoylmyristic acid; analogous sites on the reducing glucosamine were acylated by 3-hydroxymyristic acid. Hydroxyl groups at C4 and C6' in the free lipid A were unsubstituted, with C6 being the proposed attachment site of the polysaccharide moiety. Chemical analysis revealed the presence of glycine in the intact LPS; its exact location in the A. actinomycetemcomitans LPS is still to be determined. Both intact LPS and free lipid A were highly lethal to galactosamine-sensitized mice, comparable to that of Salmonella.
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PMID:Investigation of the structure of lipid A from Actinobacillus actinomycetemcomitans strain Y4 and human clinical isolate PO 1021-7. 191 49

The development and persistence of Salmonella-specific serum antibodies of different immunoglobulin classes and subclasses were compared between those who developed reactive arthritis (n = 39) and those who did not (n = 58) after Salmonella infection. Antibodies against lipopolysaccharide and SDS-extract antigen were measured by ELISA. A significant difference was seen between the two patient groups after 4-14 months of follow-up; those with reactive arthritis had higher levels of Salmonella-specific IgM, IgG, and IgA class antibodies than those without arthritis. In the increased antibody response, secretory IgA, IgA1, and IgG2 classes were especially well represented. The persisting antibody response is a common feature in reactive arthritis and supports persistence of the pathogen or its components in the host. The differences observed in antibody profiles between Salmonella- and Yersinia-triggered reactive arthritides suggest certain dissimilarities (e.g., in the location of persisting microbes) in the arthritogenic process due to these two microbes.
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PMID:Salmonella-specific antibodies in reactive arthritis. 195 13


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