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)

A transformed bovine peritoneal macrophage cell line was developed and characterized. Primary peritoneal macrophages were transformed by calcium-phosphate transfection with SV40 plasmid DNA. The transformed cell line retained the morphology of resident peritoneal macrophages as determined by light microscopy and histochemical analysis showed non-specific esterase activity. In addition, immunohistochemical staining of transformed peritoneal macrophages for lysozyme activity was positive. Transformed cells phagocytized Staphylococcus aureus, lysed chicken red blood cell (RBC) targets with and without opsonization and produced hydrogen peroxide radicals and interleukin-6 upon stimulation with opsonized zymosan and lipopolysaccharide, respectively. Transformed cells were also able to ingest and kill Mycobacterium paratuberculosis, an acid-fast bacillus. These results suggest that this cell line should be useful to study interactions between the bovine and intracellular pathogens.
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PMID:Immortalization and characterization of bovine peritoneal macrophages transfected with SV40 plasmid DNA. 767 7

After an intravenous injection of E. coli endotoxin in dogs a decrease in cerebral blood flow (CBF) and an increase in cerebral metabolic rate of oxygen (CMRo2) have been shown to occur. In metabolic acidosis following endotoxin CMRo2 increased with decreasing pH. A possible explanation for the increased CMRo2 after endotoxin and metabolic acidosis seems to be a damage of the blood-brain barrier (BBB) by endotoxin. This gives possibilities for a leakage of hydrogen ions and circulating monoamines from the blood to the brain, thus affecting the cerebral blood flow and metabolism. The effects of an E. coli endotoxin injection on CBF and CMRo2 during metabolic acidosis and beta-adrenoceptor blockade were studied in eight anaesthetized dogs. All the dogs were pretreated with propranolol (PPL), per os 12.5 mg.kg-1 twice a day for one week. Metabolic acidosis (pH 7.01-7.30) was achieved by an intravenous infusion of hydrochloric acid. Endotoxin E. coli lipopolysaccharide O 111:B 4 was given as an intravenous injection of 1 mg.kg-1 bodyweight over a 5 min period. Another five animals, published earlier, with the same experimental protocol but without PPL, constituted a control group. After endotoxin no increase in CMRo2 or CBF was observed with increasing acidosis in the PPL-group. In the control group, after endotoxin, both CBF and CMRo2 increased with decreasing pH. This resulted in a significant difference in both CBF and CMRo2 between the groups in the pH range 7.01-7.15. The present results indicate that the increase in CMRo2 and CBF with metabolic acidodis in endotoxinaemia is mediated via beta-adrenoceptors.
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PMID:Effects of propranolol pretreatment on cerebral blood flow, oxygen uptake and catecholamines during metabolic acidosis following E. coli endotoxin in dogs. 767 80

In this study we examined the effect of myelin P2 protein on some proinflammatory functions exerted by human mononuclear phagocytes. Northern blot analysis demonstrated that P2 protein selectively induced in monocytes and macrophages mRNA accumulation of tumor necrosis factor (TNF), interleukin 1 beta (IL-1 beta), and interleukin 8 (IL-8) in a time-dependent manner. Natural killer stimulating factor (IL-12) mRNA and protein secretion was strongly induced by lipopolysaccharide but not by P2 protein. Supernatants harvested from P2-stimulated monocytes contained significant amounts of TNF, IL-1 beta, and IL-8, whereas those from macrophages contained only TNF and IL-8. The effect of the P2 protein on TNF and IL-8 mRNA accumulation and secretion was not affected by polymyxin B, which, on the other hand, almost completely abolished the effect of lipopolysaccharide. Finally, P2 protein did not directly trigger hydrogen peroxide release but, through the induced release of TNF, potentiated monocyte respiratory burst capability. Since P2 protein is the antigen responsible for the induction of experimental allergic neuritis, these findings identify a potential mechanism involved in the inflammatory reaction and myelin damage during experimental allergic neuritis.
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PMID:Production of tumor necrosis factor and other proinflammatory cytokines by human mononuclear phagocytes stimulated with myelin P2 protein. 768 3

The O-specific side-chain of the lipopolysaccharide from Escherichia coli O127a:H- (O127a:4932-53) has been investigated using 2D NMR spectroscopy, methylation analysis, and partial solvolysis with anhydrous hydrogen fluoride as the principal methods. It is concluded that the polysaccharide is composed of tetrasaccharide repeating-units having the following structure. -->2)-alpha-L-Fucp-(1-->2)-beta-D-Galp-(1-->3)-alpha-D-GalpNAc-(1- ->3)-alpha-D- GalpNAc-(1--> The polysaccharide contains approximately one mole of O-acetyl groups per repeating unit distributed over several positions.
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PMID:Structural studies of the Escherichia coli O127 O-antigen polysaccharide. 769 48

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1 alpha, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor alpha in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO-fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.
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PMID:Effects of dietary lipid manipulation upon inflammatory mediator production by murine macrophages. 775 22

Recent studies have shown that surface epithelial cells play a major role in the defence and inflammatory reactions of the airways. How extracellular stimuli lead to increased gene expression in these epithelial cells is not well known. In this study, we asked whether the multiunit transcription factor, nuclear factor (NF)-kappa B, which regulates the expression of genes involved in defense and immune processes, is activated in airway epithelial cells following stimulation with inflammatory mediators and hydrogen peroxide. In addition, we studied whether this would be followed by upregulation of the NF-kappa B target gene product granulocyte-macrophage colony-stimulating factor (GM-CSF). Activation of NF-kappa B in the SV40 transformed human tracheobronchial epithelial cell line 1HAEo- was measured by electrophoretic mobility shift assays. GM-CSF concentrations in cell culture supernatants were determined by enzyme-linked immunosorbent assays. NF-kappa B was rapidly activated by exposure of cells to interleukin-1 beta (IL-1 beta), phorbol myristate acetate (PMA), and tumour necrosis factor-alpha (TNF). Exposure to H2O2 platelet activating factor (PAF) and lipopolysaccharide (LPS) did not lead to increased NF-kappa B activation. Co-stimulation of IL-1 beta with H2O2 led to augmentation and prolongation of the effect on NF-kappa B activation compared to stimulation with IL-1 beta alone. GM-CSF concentrations increased following stimulation with IL-1 beta and H2O2, and the effect of IL-1 beta/H2O2 co-stimulation on GM-CSF concentrations was additive. These results suggest that NF-kappa B may represent an important transcription factor, controlling the expression of cytokine genes in airway epithelial cells.
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PMID:Activation of the transcription factor NF-kappa B in human tracheobronchial epithelial cells by inflammatory stimuli. 778 82

Ileus is common during sepsis; however, the etiology of this gastrointestinal dysmotility is unclear. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal motility, gastric emptying, gastric acid secretion, and colonic transit. Six dogs underwent placement of manometric catheters in the stomach and small bowel and insertion of a gastric and a cecal cannula. After the animals recovered, fasting and fed gastrointestinal motility was recorded, and gastric emptying and colonic transit were studied with nonabsorbable liquid and solid markers, respectively. Following completion of baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg intravenously) and the studies were repeated on Postendotoxin Days 1-3. The single bolus of endotoxin abolished the migrating motor complexes, decreased the fasting motility index, decreased hydrogen ion output, slowed liquid gastric emptying, and prolonged colonic transit for 2 days. Gastrointestinal motility and transit returned to baseline on Postendotoxin Day 3. In conclusion, a single, sublethal dose of endotoxin temporarily disrupts fasting and postprandial canine gastrointestinal motility and transit.
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PMID:Effect of endotoxin on canine gastrointestinal motility and transit. 783 Apr 12

The monoclonal antibody YsT9.1 is specific for the lipopolysaccharide A antigen of Brucella abortus. A complex formed between the Fab of YsT9.1 (Ab1) and the Fab of its antidiotopic monoclonal antibody T91AJ5 (Ab2) has been crystallized, and data have been collected to 2.8 A resolution. The space group is monoclinic P2(1), with one molecule per asymmetric unit. The structure was solved using a limited Patterson-correlation search over the asymmetric-unit of rotation space, and has been refined to an R-factor of 0.174. The complex is a head-to-head dimer, with the contact between the two Fabs almost completely restricted to their hypervariable loops. The interactions between the two Fabs in the complex are dominated by tyrosine residues, not only in the formation of hydrogen bonds, but in their participation in an aromatic ring network that spans the two Fv domains. The anti-idiotope was found to be unable to carry an internal image of the antigen and induce polysaccharide-specific "anti-anti-idiotopes" (Ab3) because the polysaccharide binding cleft on the Ab1 is too narrow and deep to allow comprehensive contact with the binding site of Ab2. The antibody T91AJ5 therefore is a class gamma anti-idiotope. The contact surfaces of the two Fabs are highly complementary; however, they are distinctly different in character. Each Fab has two separate binding surfaces of approximately equal size, but while the two binding surfaces of Ab1 are partitioned between the light and heavy chains, the two binding surfaces of Ab2 are shared between the chains, with the heavy chain responsible for about 60% of the total binding area. The structure of the unliganded Fab of Ab2 has also been solved by molecular replacement, and refined to an R-factor of 0.152 at 2.8 A resolution. This Fab crystallizes in the orthorhombic space group P2(1)2(1)2(1), with one molecule per asymmetric unit. The second hypervariable loop of the heavy chain of the Ab2 Fab is observed to undergo a significant and necessary conformational rearrangement in going from the unliganded to complexed form, and thus complex formation is an example of "induced fit" of antigen to antibody. The unliganded Ab1 Fab packs in the standard head-to-tail fashion observed for other Fabs. This mode of packing is precluded in the complex, by its head-to-head nature, and it is found to pack in tilted layers with most intermolecular contacts made between adjacent Ab2 Fab molecules.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exploring the mimicry of polysaccharide antigens by anti-idiotypic antibodies. The crystallization, molecular replacement, and refinement to 2.8 A resolution of an idiotope-anti-idiotope Fab complex and of the unliganded anti-idiotope Fab. 807 93

Endotoxemia is associated with enhanced release of a variety of cytotoxic and/or proinflammatory mediators from locally activated tissue macrophages. The lung is highly sensitive to damage induced by endotoxin, suggesting that pulmonary macrophages are activated by this bacterially derived product to release mediators that contribute to the pathogenesis of tissue injury. In the present studies, we used a rat model of acute endotoxemia induced by a single intravenous injection of animals with lipopolysaccharide (LPS) to determine the extent to which different lung macrophage subpopulations are activated. Alveolar macrophages (AM) and interstitial macrophages (IM) were isolated sequentially from the lung by lavage, followed by digestion with collagenase and selective adherence to tissue culture dishes. Both AM and IM were found to produce superoxide anion, as well as hydrogen peroxide in response to inflammatory stimuli. AM produced greater quantities of these reactive oxygen intermediates than did IM. Treatment of rats with LPS resulted in a significant increase in production of reactive oxygen intermediates by IM, but not by AM. Similarly, while AM from untreated rats phagocytized more opsonized sheep red blood cells than did IM, LPS treatment of rats significantly enhanced phagocytosis only in IM. In addition, this treatment caused a significant increase in chemotaxis of IM towards C5a. In contrast, although LPS treatment of rats had no effect on tumor necrosis factor-alpha release by AM, a significant reduction was observed in IM. Taken together, these data demonstrate that IM play a role in the inflammatory response of the lung to acute endotoxemia.
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PMID:Enhanced phagocytosis, chemotaxis, and production of reactive oxygen intermediates by interstitial lung macrophages following acute endotoxemia. 808 72

Sinomenine, an epimorphinan alkaloid, was tested for protecting hepatitis induced by lipopolysaccharide (LPS) in galactosamine (GalN)-sensitized mice. Sinomenine protected against the hepatic injuries in the dose range of 10-100 mg/kg in a dose-dependent manner and suppressed the production of tumor necrosis factor (TNF), which appeared in serum earlier than aminotransferases in GalN/LPS-treated mice. Sinomenine significantly suppressed the in vitro production of superoxide anion and hydrogen peroxide in the macrophage cultures stimulated with phorbol 12-myristate acetate. It is discussed that sinomenine prevents GalN/LPS-treated hepatic failure by suppressing TNF production and/or reactive oxygen generation.
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PMID:Protection by sinomenine against endotoxin-induced fulminant hepatitis in galactosamine-sensitized mice. 809 93


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