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)

Tumor necrosis factor is a cytokine that mediates many of the biologic actions of endotoxin. Recent studies have shown that tumor necrosis factor administration may cause liver injury and that tumor necrosis factor may mediate the lethality of the hepatotoxin galactosamine. One of the most potent inducers of tumor necrosis factor production is endotoxin. Because patients with alcoholic liver disease frequently have endotoxemia and because many of the clinical manifestations of alcoholic hepatitis are known biologic actions of tumor necrosis factor, we thought it would be important to evaluate tumor necrosis factor activity in patients with alcoholic hepatitis. Basal and lipopolysaccharide-stimulated tumor necrosis factor release from peripheral blood monocytes, a major source of tumor necrosis factor production, was determined in 16 patients with alcoholic hepatitis and 16 healthy volunteers. Eight of 16 alcoholic hepatitis patients and only two of 16 healthy volunteers had detectable spontaneous tumor necrosis factor activity (p less than 0.05). After lipopolysaccharide stimulation, mean monocyte tumor necrosis factor release from alcoholic hepatitis patients was significantly increased to over twice that of healthy controls (25.3 +/- 3.7 vs. 10.9 +/- 2.4 units per ml, p less than 0.005). We conclude that monocytes from alcoholic hepatitis patients have significantly increased spontaneous and lipopolysaccharide-stimulated tumor necrosis factor release compared to monocytes from healthy volunteers. We suggest that some of the metabolic abnormalities and possibly some of the liver injury of alcoholic hepatitis may be due to enhanced tumor necrosis factor production.
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PMID:Increased tumor necrosis factor production by monocytes in alcoholic hepatitis. 292 Sep 91

Studies of turkey poult responses to Pasteurella multocida endotoxins indicated that lipopolysaccharide (LPS) preparations from two highly pathogenic strains and free endotoxin from one of these strains were all similar in lethal toxicity. Lethal intravenous doses were generally high, 1 mg or more for 1-week-old poults (13.3 mg/kg). The toxic effects of LPS were not increased by repeated administration of small hourly doses. For both forms of endotoxin, the relationship between dose and response was considered erratic. Attempts to increase the susceptibility of poults to LPS by administering a liver-damaging substance (galactosamine) or a histamine-releasing substance (compound 48/80) or by performing surgical bursectomy were not effective. The LPS did not provoke a dermal Shwartzman reaction, even though doses used were 10 times those that produced a characteristic reaction in a rabbit.
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PMID:Effects of Pasteurella multocida endotoxins on turkey poults. 296 Mar 11

To elucidate the function of the reticuloendothelial system of liver in hepatic injury, we investigated the effect of endotoxins on superoxide anion (O-2) generating capacity and lysosomal enzyme activities of Kupffer cells isolated from rats treated with galactosamine (Gal N), with Gal N supplemented with polymyxin B (Polymyxin B-Gal N), with lipopolysaccharide (LPS) and from control rats. After collagenase digestion of the liver and centrifugation over metrizamide gradient, Kupffer cells were prepared by the dish adherence procedure. O-2 production by the cells was examined as chemiluminescence during phagocytosis of latex particles and beta-glucuronidase activities were analyzed. High titers of endotoxemia were detected in LPS and Gal N rats by limulus test, while a low endotoxemia titer was found in Polymyxin B-Gal N rats. Hepatocyte damage was found in Gal N rats, but little was recognized in LPS and Polymyxin B-Gal N rats. In the latter groups, Kupffer cells, activated by endotoxins, showed the enhancement of chemiluminescence and a release of lysosomal enzyme. Though lysosomal enzyme was released from Kupffer cells in Gal N rats, chemiluminescence was slightly suppressed in spite of the high titer of endotoxemia. These results appear to be related to the consumption of O-2 during liver injury. The functional state of Kupffer cells was thus changed by the grade of endotoxemia and hepatic injury.
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PMID:Superoxide anion generating capacity and lysosomal enzyme activities of Kupffer cells in galactosamine induced hepatitis. 301 77

Veillonellophage N2 prevented from adsorbing to Veillonella rodentium ATCC 17743 cells treated with polymyxin B, and also to lipopolysaccharides (LPSs) of the host cells treated with antibiotics. Therefore, these results indicate that receptor to phage N2 is cell wall LPSs. The LPSs of V. rodentium ATCC 17743 cells as receptor were characterized. Lipid A and total carbohydrate accounted for approximately 40% of the weight of the lipopolysaccharide complex. Heptose and 2-keto-3-deoxyoctonate were also present. Amino compounds included glucosamine, galactosamine, and glycine.
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PMID:Phage-receptor on the cell wall of Veillonella rodentium. 304 3

Structural studies were carried out on a rhamnose-rich polysaccharide isolated from the O-polysaccharide fraction of lipopolysaccharide in Pseudomonas aeruginosa IID 1008 (ATCC 27584) after destruction of the major O-specific chain by alkaline treatment. The isolated polysaccharide contained rhamnose, 3-O-methyl-6-deoxyhexose, glucose, xylose, alanine, galactosamine and phosphorus in a molar ratio of 67:6.9:4.3:2.1:1.1:1.0:4.1. Data from analysis involving Smith degradation, methylation, 1H-NMR spectroscopy and optical rotation measurement showed that the polysaccharide was built up of three moieties, a rhamnan chain composed of about 70 D-rhamnose residues, the core chain and an oligosaccharide chain comprising 3-O-methyl-6-deoxyhexose, xylose, rhamnose and probably glucose. The repeating unit of the rhamnan chain was indicated to have the following structure:----3)D-Rha(alpha 1----3)D-Rha(alpha 1----2)D-Rha(alpha 1----. This structure is identical with that proposed previously for the repeating unit of the side chain of lipopolysaccharide from plant pathogenic bacteria Pseudomonas syringae pv. morsprunorum C28 [Smith, A.R.W., Zamze, S.E., Munro, S.M., Carter, K. J. and Hignett, R.C. (1985) Eur. J. Biochem. 149, 73-78].
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PMID:Characterization of a polysaccharide component of lipopolysaccharide from Pseudomonas aeruginosa IID 1008 (ATCC 27584) as D-rhamnan. 311 49

Antitumor activity of three derivatives of chemically synthesized diacyloxyacylglucosamine-4-phosphate (acyl-GlcN-4P) linked 3-deoxy-D-manno-2-octulosonic acid (KDO) and 12 derivatives of acyl-GlcN-4P or acyloxyacylglucosamine-6-phosphate (acyl-GlcN-6P) with chiral acyloxyacyl groups at the C-2 and C-3 positions was examined. Ehrlich carcinoma cells (1 x 10(4] were inoculated i.p. into ddY mice on day 0, and these compounds (100 micrograms/d/mouse) were administered i.p. on days -5, -2, +1, +3, and +5. Although the antitumor activity of the acyl-GlcN-4P linked KDO was weaker than that of the natural lipopolysaccharide, groups of mice administered A-301 with di-3-hexadecanoyloxytetradecanoyl [(R)C14-O-C16] at C-2, -3, and A-303 with di-3-tetradecanoyloxytetradecanoyl [(R)C14-O-C14] showed longer mean survival times than the control group. However, KDO-attachment appeared not to enhance the antitumor activity of acyl-GlcN-4P. The group of mice administered acyl-GlcN-4P (A-145) or acyl-GlcN-6P (A-144 and A-146), which have an acyloxyacyl group at C-2, -3, showed prolonged survival times when compared to the control group, but the differences were not significant. On the other hand, when compound A-107 with [(S)C14-O-C14] at the C-2 position and 6-phosphate was administered to 5 mice, 3 mice survived for 25 d. Furthermore, mitogenicity for splenocytes of C57BL/6 mice and lethal toxicity in C57BL/6 mice sensitized with D-galactosamine were observed with the acyl-GlcN-4P or -6P derivatives with (R) or (S) isomers of fatty acid.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antitumor activity, mitogenicity, and lethal toxicity of chemically synthesized monosaccharide analogs of lipid A. 318 27

Tumor necrosis factor (TNF) has been shown to mediate lipopolysaccharide-induced neutrophil adhesion to liver sinusoidal endothelium in vivo. Female NMRI mice received either 5 micrograms lipopolysaccharide (R595) per animal alone (model A) or together with 116 mumol D-galactosamine (model B). One hour after injection, TNF activity in the serum was detectable to an equal extent in both models. Neutrophils in the liver, which had been identified by chloroacetate esterase staining of liver sections and quantitated by light microscopy, started to increase at 1 h and were elevated 10-fold above baseline at 6 h after application in (A) and (B). If 0.5 micrograms TNF instead of lipopolysaccharide was injected alone (model C) or together with D-galactosamine (model D), neutrophil influx into the liver was comparable to that observed in (A) or (B). Alanine aminotransferase activity in the serum was nearly normal in (A) and (C) 6 h after injection, while it reached levels up to 50-fold above baseline in models (B) and (D). This reflects the well-known D-galactosamine sensitization against lipopolysaccharide or TNF. Furthermore, degranulation of a large number of intrasinusoidal neutrophils could be observed 9 h after lipopolysaccharide-galactosamine injection. The administration of 116 mumol D-galactosamine per animal alone led neither to a measurable TNF activity in the serum nor to an increase in alanine aminotransferase activity or number of liver neutrophils. If the animals had received 50 microliter turpentine subcutaneously 24 h prior to lipopolysaccharide, TNF or D-galactosamine injection, the induced acute-phase reaction suppressed the increase of liver neutrophils in all models. Acute-phase reaction also prevented neutrophil degranulation and the rise of alanine aminotransferase in (B) to a great extent, while serum TNF activity was only minimally affected. It is concluded that TNF mediates neutrophil adhesion to the sinusoidal endothelium in vivo and that acute-phase reactants prevent lipopolysaccharide- or TNF-induced neutrophil influx into the liver.
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PMID:Involvement of tumor necrosis factor in endotoxin-triggered neutrophil adherence to sinusoidal endothelial cells of mouse liver and its modulation in acute phase. 319 26

The cellular and subcellular distribution of biologically tritiated Salmonella abortus equi lipopolysaccharide (LPS) was studied at different time intervals after intravenous injection in rats. At 1 min after injection of LPS via the portal vein label was present over Kupffer cell phagosomes. Between 30 min and 7 days after injection, silver grains were mainly associated with phagosomes and lysosomes and occasionally with the membrane of Kupffer cells. A few parenchymal cells were labeled at 5 min in their mitochondria, cell membrane and the periphery of the cell. Radioactivity was also present in the rough endoplasmic reticulum (from 15 min), fat droplets and the nucleus (from 3 h) up to 7 days. Sinusoidal endothelial and fat-storing cells were never labeled. In conclusion, both Kupffer cells and parenchymal cells play a role in the uptake of LPS by the liver. The uptake and processing of endotoxin is rapid, since label is found early after administration and radioactivity is detected in the bile within 1 h. This radioactivity represents non-detoxified LPS, since it is lethal for galactosamine-sensitised mice after extraction with hot phenol/water. However, in the presence of bile salts, the LPS is non-lethal and not capable of clotting the limulus amebocyte lysate. LPS injection causes bile flow reduction within 45 min.
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PMID:Cellular and subcellular distribution of injected lipopolysaccharide in rat liver and its inactivation by bile salts. 323 1

A lipopolysaccharide was isolated from Pseudomonas aurantiaca IMB 31 by extraction with aqueous phenol and purified by ultracentrifugation. The lipopolysaccharide was confined to the phenol phase. Fucosamine (2-amino-2,6-dideoxygalactose) (36%) and bacillosamine (2,4-diamino-3,4,6-trideoxyglucose) (23%) were identified as hypothetic components of the O-chain in the carbohydrate moiety of the macromolecule using the techniques of paper chromatography, gas-liquid chromatography and ion-exchange chromatography on an amino acid analyser. Rhamnose, glucose, galactose, glucosamine and galactosamine were detected as hypothetical components of the core in the lipopolysaccharide composition, as well as 2-keto-3-deoxyoctonic acid, heptose, alpha-alanine and phosphorus, usual components of the core in Pseudomonas. The following predominant fatty acids were identified in the composition of lipid A using the techniques of gas-liquid chromatography with standard compounds and gas-liquid mass spectrometry: 3-OH C10:0 (14.4%), C12:0 (30.5%), 2-OH C12:0 (14.9%), 3-OH C12:0 (17.4%), C16:0 (9.9%). The serological relationship between P. aurantiaca strains was studied, and their phylogenetic relationship with P. fluorescens is discussed.
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PMID:[Immunochemical characteristics of a lipopolysaccharide from Pseudomonas aurantiaca]. 324 96

Polyamines and acetylpolyamines were analyzed in the liver, spleen, lung, kidney, serum and urine by high-performance liquid chromatography on a column of cation-exchange resin after administering various cytotoxic substances to male mice. All of the compounds tested more or less affected the tissue levels of polyamines, including putrescine, spermidine, spermine and acetylpolyamines (N1-acetylspermidine and N1-acetylspermine). It was found that they were classified into two groups of substances: one group (including radical-producing drugs and lipopolysaccharide) which elevated the tissue levels of N1-acetylspermidine, especially in the liver, while another group of drugs (such as D-galactosamine and DL-ethionine) had little effect on the acetylpolyamine levels. When the acetylpolyamine levels rose, the levels of spermidine and spermine declined, and then putrescine levels were elevated. N1-Acetylspermine was detected only when N1-acetylspermidine levels were very high after treatment with radical-producing drugs and lipopolysaccharide. Halogenated carbon, such as carbon tetrachloride and halothane, elevated the levels of acetylpolyamines especially in the liver, while paraquat elevated them in all tissues examined.
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PMID:Elevation of acetylpolyamine levels in mouse tissues, serum and urine after treatment with radical-producing drugs and lipopolysaccharide. 335 6


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