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

The specific polysaccharide was released from Shigella dysenteriae type 5 lipopolysaccharide by mild acidic hydrolysis and then purified by gel chromatography on Sephadex G-50. The polysaccharide was built up of residues of D-mannose, 2-acetamido-2-deoxy-D-glucose, 3-0-(D-1-carboxyethyl)-L-rhamnose (rhamnolactylic acid) and 0-acetyl groups in a ratio 2:1:1:1. On the basis of radiospectroscopy, methylation analysis, Smith degradation, and chromium trioxide oxidation, the repeating oligosaccharide unit of the polysaccharide can be assigned the following structure: (formula: see text) where GlcNAc is 2-acetamido-2-deoxy-D-glucopyranose, Manp is mannopyranose, RhaLcA is rhammolacytic acid and Ac is an acetyl group. The serological properties of Sh. dysenteriae somatic antigens are discussed in relation to the chemical structures of their specific polysaccharides.
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PMID:Somatic antigens of Shigella. The strucuture of the specific polysaccharide chain of Shigella dysenteriae type 5 lipopolysaccharide. 33 37

Addition of small amounts of chromium chloride to a saline suspension of Salmonella typhosa lipopolysaccharide (LPD; Difco) caused a marked reduction in several of the biologic activities of this substance including toxicity, B-cell mitogenicity, plasma colony-stimulating activity (CSA), radioprotective effect, and induction of the dermal Shwartzman reaction. Nevertheless, LPS treated with chromium chloride was found to be at least as effective as untreated LPS in enhancing resistance of B6CBF1 mice to the lethal effects of Klebsiella pneumoniae infection.
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PMID:Biologic properties of bacterial lipopolysaccharides treated with chromium chloride. 35 Mar 61

The specific polysaccharide was obtained from the lipopolysaccharide of Shigella newcastle by mild acid hydrolysis and further purified by permeation chromatography on Sephadex G-50. It was found to consist of L-rhamnose, 2-acetamido-2-deoxy-D-galactose, D-galacturonic acid residues and O-acetyl groups in the molar ratios of 2:1:1:1. On the basis of 1H and 13C nuclear magnetic resonance spectroscopy, methylation analysis, partial acid hydrolysis, Smith degradation, and chromium trioxide oxidation, the following structure can be assigned to the repeating oligosaccharide unit of the polysaccharide:-4)DGalA(beta 1-3)DGalNAc-(beta 1-2)LAc3Rha(alpha 1-2)LRha(alpha 1-, where GalA = galacturonic acid. GalNAc = N-acetylgalactosamine, Ac3Rha = 3-O-acetylrhamnose. The structural and immunochemical data presented prove that Sh. newcastle lipopolysaccharide belongs to a 'non-classical' type of somatic antigens with acidic O-specific polysaccharide chains.
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PMID:Somatic antigens of Shigella. The structure of the specific polysaccharide of Shigella newcastle (Sh. flexneri type 6) lipopolysaccharide. 38 Oct 1

A lipopolysaccharide has been isolated from Pseudomonas maltophilia N.C.T.C. 10257. Monosaccharide components identified were L-rhamnose, 3-O-methyl-L-xylose, L-xylose, D-glucose, D-mannose, D-galacturonic acid, 2-amino-2-deoxy-galactose, 2-amino-2-deoxyglucose, and a 3-deoxy-2-octulosonic acid. Heptose was absent. In this and other respects, the lipopolysaccharide resembles the corresponding products from Xanthomonas species. Mild hydrolysis of the lipopolysaccharide with acid, followed by chromatography of the water-soluble products on Sephadex G-50, gave a polymeric, "side-chain" fraction containing rhamnose, 3-O-methylxylose, and xylose residues in the molar rations approximately 15:4:1. Methylation analysis, periodate oxidation, Smith degradation, and oxidation with chromium trioxide were the principal methods used in the study of this fraction. The following structure is proposed for the characteristic repeating-unit of the polymer.
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PMID:Lipopolysaccharides from Pseudomonas maltophilia: structural studies of the side-chain polysaccharide from strain N.C.T.C. 10257. 42 32

The core oligosaccharide isolated from the lipopolysaccharide of Aeromonas salmonicida ssp. salmonicida has been investigated by methylation analysis, NMR spectroscopy (13C and 1H), oxidation with periodate and chromium trioxide, and Smith degradation. The following structure is proposed: [Formula: see text]
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PMID:Structure of the core oligosaccharide in the lipopolysaccharide isolated from Aeromonas salmonicida ssp. salmonicida. 139 31

Intravenous lipopolysaccharide (LPS) decreases superior mesenteric arterial blood flow and increases ileal mucosal permeability in pigs. We tested the hypothesis that these phenomena can be ameliorated by pretreatment and posttreatment with ibuprofen. Pentobarbital-anesthetized immature swine were mechanically ventilated (fraction of inspired oxygen, 0.5) and infused with Ringer's lactate (RL) solution (0.8 mL/kg per minute). Animals in group RL (n = 10) received no other interventions. Animals in group RL + LPS (n = 15) were infused with LPS (50 micrograms/kg) from a time range equal to 0 through 60 minutes. Animals in group RL + LPS + ibuprofen (n = 10) were similarly infused with LPS, but in addition, they received ibuprofen (10 mg/kg at -30 minutes and 10 mg/kg per hour from -30 through 210 minutes). Intestinal permeability was assessed by measuring plasma-to-lumen clearances of two hydrophilic probes (chromium 51-labeled edetic acid monohydrate [EDTA] and urea) and by expressing the results as a clearance ratio (CEDTA/CUREA). Survival was 100%, 67%, and 100% in groups RL, RL + LPS, and RL + LPS + ibuprofen, respectively. Among survivors only, CEDTA/CUREA increased significantly over time in both endotoxic groups, but not in nonendotoxic controls. Treatment with ibuprofen transiently blocked LPS-induced mesenteric hypoperfusion. These data indicate that mediators other than cyclooxygenase-derived metabolites of arachidonic acid are responsible for the adverse effect of LPS on mesenteric permeability to hydrophilic solutes in this porcine model.
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PMID:Ibuprofen improves survival but does not ameliorate increased gut mucosal permeability in endotoxic pigs. 173 50

The purpose of this in vitro study was to determine whether Pasteurella haemolytica capsular extract (CE) damages bovine pulmonary endothelial cells (EC) directly or through neutrophil-mediated mechanisms. Chromium 51-labeled EC were treated with the following variables: CE (1, 10, and 100 ng of protein/ml), CE and bovine neutrophils (10(6) cells/well), and CE and polymyxin B (500 U/ml). Although only minimal damage to EC occurred by 5 hours after treatment, by 22 hours after treatment, the 10-ng and 100-ng CE dose produced severe damage to EC, as indicated by 51Cr release, cellular detachment, and loss of monolayer confluency. The component in the CE that was toxic to the EC was lipopolysaccharide, evidenced by effective neutralization of the toxic effect with polymyxin B. Neutrophils inhibited the CE-mediated EC toxicity and were activated, as indicated by shape change and adhesion to EC monolayers. We concluded that the lipopolysaccharide component of CE causes direct damage to EC, which can be attenuated by neutrophils and polymyxin B.
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PMID:Effect of Pasteurella haemolytica saline capsular extract on bovine pulmonary endothelial cells. 178 21

Infusing pigs with lipopolysaccharide (LPS) decreases superior mesenteric artery blood flow (Qsma), suggesting that mesenteric hypoperfusion may be responsible for LPS-induced alterations in gut mucosal permeability. To test this hypothesis, we studied four groups of anesthetized swine. Group 1 animals (N = 6) were infused with LPS (250 micrograms/kg over 1 hour beginning at 60 minutes) and continuously resuscitated with Ringer's lactate (48 mL/kg per hour). In group 2 (N = 5), Qsma was decreased by 50% by means of a mechanical occluder to mimic the LPS-induced alterations in Qsma observed in group I. Group 3 (N = 5) was included to document our ability to detect ischemia/reperfusion-induced alterations in mucosal permeability; in these pigs, Qsma was decreased in steps to zero flow (at 150 to 210 minutes) and then perfusion was restored (at 210 to 270 minutes). Pigs in group 4 (N = 6) served as normal controls; these animals were resuscitated with Ringer's lactate at the same rate as in group 1 but were not infused with LPS. To assess mucosal permeability, we measured plasma-to-lumen clearances for two markers, chromium 51-labeled edetic acid monohydrate (EDTA) and urea. Loading and maintenance infusions of the markers were given intravenously, and a 20-cm isolated segment of small intestine was continuously perfused at 2 mL/min with Ringer's lactate at 37 degrees C. Results were expressed as the ratio of the clearances for the two probes (CEDTA/CUREA). In group 3, CEDTA/CUREA was 999% +/- 355% of baseline at 270 minutes. In group 1, CEDTA/CUREA was 572% +/- 235% of baseline at 270 minutes. In groups 2 and 4, however, CEDTA/CUREA did not change significantly from the baseline value over the duration of the study. These data suggest that increased mucosal permeability after LPS is due to factors other than (or in addition to) mesenteric hypoperfusion.
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PMID:Increased intestinal permeability in endotoxic pigs. Mesenteric hypoperfusion as an etiologic factor. 189 58

Lipopolysaccharide increases intestinal mucosal permeability to hydrophilic compounds such as chromium 51-labeled edetate (51Cr-EDTA). We sought to determine whether this phenomenon is partly mediated by lipopolysaccharide-induced mesenteric hypoperfusion. We assessed permeability in an isolated segment of ileum by measuring plasma-to-lumen clearances (C) for two probes, 51Cr-EDTA and urea, and expressing the results as a ratio (CEDTA/CUREA). In control pigs (n = 6) resuscitated with Ringer's lactate (RL), mucosal permeability was unchanged during the 210-minute period of observation. In pigs (n = 7) infused with lipopolysaccharide (50 micrograms/kg) and similarly resuscitated with RL, mesenteric perfusion (Qsma) decreased significantly and permeability increased progressively and significantly. When endotoxic pigs (n = 6) were resuscitated with a regimen (RL plus hetastarch plus dobutamine) that preserved normal Qsma, lipopolysaccharide-induced mucosal hyperpermeability was prevented. Resuscitation of endotoxic pigs (n = 6) with RL plus hetastarch provided intermediate protection against both mesenteric hypoperfusion and increased permeability. These data suggest that diminished Qsma contributes to impaired ileal mucosal barrier function in experimental endotoxicosis.
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PMID:Maintenance of superior mesenteric arterial perfusion prevents increased intestinal mucosal permeability in endotoxic pigs. 190 30

Effect of zinc on an inhibitory action of cadmium to mitogen-induced lymphocyte proliferation was investigated. Cadmium at concentrations below 10 microM selectively inhibited concanavalin A-induced T-cell proliferation as compared with bacterial lipopolysaccharide-induced B-cell proliferation. Such differential susceptibility of T- and B-cell proliferation was not observed in the cases of other cations such as mercury, lead, nickel, molybdenum, chromium(VI) and arsenic (V). The inhibitory effect of 10 microM cadmium on T-cell proliferation was almost completely prevented by addition of 30 microM zinc to the culture medium, but was not by ferrous iron, nickel and copper. Further, cadmium exerted the same extent of inhibition even when it was added at 16 h after concanavalin A stimulation, and thereafter the inhibition gradually decreased. Correlated well with this observation, the protective effect of zinc was seen as far as it existed during the first 16 h of the mitogen stimulation. As intracellular cadmium content and a cadmium-induced metallothionein level were not changed by zinc addition, these observations strongly suggest that cadmium inhibits some zinc-dependent processes required for T-cell proliferation.
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PMID:Differential susceptibility of T- and B-lymphocyte proliferation to cadmium: relevance to zinc requirement in T-lymphocyte proliferation. 204 24


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