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)

Calcitonin gene-related peptide (CGRP), a potent vasodilator, and neuropeptide Y (NPY), a potent vasoconstrictor and potentiator of norepinephrine-induced vasoconstriction, were examined in an animal model of endotoxin shock. Gram-negative bacterial endotoxin (lipopolysaccharide B from Salmonella enteritidis) was administered as a bolus (16.7 mg/kg, i.v.) to conscious, unrestrained rats, previously cannulated for blood pressure measurements and blood withdrawal. At 30 min, endotoxin caused 35-40 mm Hg drop in mean arterial pressure and significant increases in heart rate and plasma levels of glucose and lactate. By 3 hr, blood pressure had returned to near normal levels and remained normal until cardiovascular collapse at 4-6 hr (approximately 70% of the rats). Endotoxin elevated plasma CGRP levels by fourfold at 30 min and 22-fold at 3 hr. Of the organs tested, only vena cava showed significant decreases in CGRP levels. Endotoxin also elevated plasma NPY levels by 67% and decreased NPY levels in adrenal gland and vena cava at 30 min and 3 hr. The data suggest that both CGRP and NPY are released into the circulation during development of endotoxin shock in the rat. NPY may contribute to the compensatory mechanism, tending to bring arterial pressure back to normal levels during intermediate stages of endotoxemia. CGRP, because of its extremely high potency as a hypotensive agent, may contribute to the hypotension at both early and late stages during pathogenesis of endotoxin shock.
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PMID:Calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) levels are elevated in plasma and decreased in vena cava during endotoxin shock in the rat. 155 Nov 83

Quantification of intracellular and extracellular levels and production rates of reactive oxygen species is crucial to understanding their contribution to tissue pathophysiology. We measured basal rates of oxidant production and the activity of xanthine oxidase, proposed to be a key source of O2- and H2O2, in endothelial cells. Then we examined the influence of tumor necrosis factor-alpha and lipopolysaccharide on endothelial cell oxidant metabolism, in response to the proposal that these inflammatory mediators initiate vascular injury in part by stimulating endothelial xanthine oxidase-mediated production of O2- and H2O2. We determined a basal intracellular H2O2 concentration of 32.8 +/- 10.7 pM in cultured bovine aortic endothelial cells by kinetic analysis of aminotriazole-mediated inactivation of endogenous catalase. Catalase activity was 5.72 +/- 1.61 U/mg cell protein and glutathione peroxidase activity was much lower, 8.13 +/- 3.79 mU/mg protein. Only 0.48 +/- 0.18% of total glucose metabolism occurred via the pentose phosphate pathway. The rate of extracellular H2O2 release was 75 +/- 12 pmol.min-1.mg cell protein-1. Intracellular xanthine dehydrogenase/oxidase activity determined by pterin oxidation was 2.32 +/- 0.75 microU/mg with 47.1 +/- 11.7% in the oxidase form. Intracellular purine levels of 1.19 +/- 1.04 nmol hypoxanthine/mg protein, 0.13 +/- 0.17 nmol xanthine/mg protein, and undetectable uric acid were consistent with a low activity of xanthine dehydrogenase/oxidase. Exposure of endothelial cells to 1000 U/ml tumor necrosis factor (TNF) or 1 microgram/ml lipopolysaccharide (LPS) for 1-12 h did not alter basal endothelial cell oxidant production or xanthine dehydrogenase/oxidase activity. These results do not support a casual role for H2O2 in the direct endothelial toxicity of TNF and LPS.
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PMID:Responses of vascular endothelial oxidant metabolism to lipopolysaccharide and tumor necrosis factor-alpha. 156 24

Glycocalyx (or slime), which is an important virulence factor of many pathogenic bacteria, was isolated from Bacteroides fragilis, Bacteroides thetaiotaomicron and Staphylococcus epidermidis. Organisms were grown for 24 h in a chemically defined, dialysable liquid medium. Bacteria were centrifuged and the supernatant was concentrated and dialysed against distilled water. Total carbohydrate and protein were estimated using standard methods. Thin layer and gas-liquid chromatography of trifluoro acetic acid hydrolysed and non-hydrolysed samples provided evidence for the presence of polysaccharide, the absence of nucleic acids and lipopolysaccharide and for the identification of the individual sugar residues. Glucose, mannose and galactose (B. fragilis), glucose (B. thetaiotaomicron), and glucose and heptose (S. epidermidis) were the sugar residues detected. Uronic acid and hexosamine were detected in all species. Glycocalyx preparations (1 mg/ml) from Bacteroides and Staphylococcus significantly inhibited the chemiluminescence and chemotactic responses of viable human polymorphonuclear leucocytes (PMNL), but were not toxic for PMNL.
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PMID:Bacteroides and Staphylococcus glycocalyx: chemical analysis, and the effects on chemiluminescence and chemotaxis of human polymorphonuclear leucocytes. 158 43

Mouse macrophages activated by interferon-gamma kill intracellular Leishmania by a process that depends on the generation of L-arginine-derived nitrogen oxidation products. Interferon-induced intracellular killing can be mimicked by exposure of macrophages to the Ca2+ ionophore A23187 in the presence of lipopolysaccharide. The mechanisms of this effect were therefore investigated. Destruction of the parasite was accompanied by accumulation of nitrite in the macrophage culture fluids. Leishmanicidal activity and nitrite production in cultures stimulated with ionophore A23187 and lipopolysaccharide were abrogated when cells were activated in medium containing arginase or the L-arginine analogues L-canavanine, guanidine or NG-monomethyl-L-arginine. L-Arginine was required during the lipopolysaccharide-induced triggering phase only. Indeed, macrophage priming with ionophore A23187 in L-arginine-depleted medium led to full microbicidal activity and nitrite generation provided that L-arginine was present during subsequent triggering by lipopolysaccharide. Addition of NG-monomethyl-L-arginine to ionophore-activated macrophages increased O2- production on phorbol myristate stimulation, while inhibiting glucose oxidation through the hexose monophosphate shunt pathway. Leishmanicidal activity and nitrite production were also inhibited when ionophore-treated cultures were incubated with excess iron, implying a role for iron as a defence mechanism against the toxicity of nitrogen derivatives. These results indicate that the ionophore-induced leishmanicidal activity occurs through a process similar to that evoked by interferon-gamma, i.e. the production of L-arginine-derived nitrogen oxidation products.
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PMID:Macrophage activation for intracellular killing as induced by a Ca2+ ionophore. Dependence on L-arginine-derived nitrogen oxidation products. 159 22

In the course of developing a live vaccine, we generated three murine monoclonal antibodies (MAb) specific for Shigella sonnei. The specificities of these MAb were determined by enzyme-linked immunosorbent assay and immunoblot analyses with whole cells or purified lipopolysaccharides (LPSs) as antigens. Two of them are specific for the Shigella serotype D O-polysaccharide determinant, whereas one specifically binds to the core hexose region of R1-type LPSs. With these MAb, it was possible to analyze clinical isolates and a hybrid Salmonella typhi strain for their expression of the corresponding LPS moieties. In addition to their use in the screening of candidate vaccine strains, the new MAb provide a powerful tool for epidemiological and phylogenetic studies of natural enterobacterial populations.
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PMID:Characterization of the Shigella serotype D (S. sonnei) O polysaccharide and the enterobacterial R1 lipopolysaccharide core by use of mouse monoclonal antibodies. 161 42

The effect of peritoneal dialysate on the capacity of peripheral blood polymorphonuclear (PMNL) and mononuclear leukocytes (MNC) to release leukotriene B4 (LTB4) and tumor necrosis factor alpha (TNF alpha) was investigated in vitro. Following density gradient separation, aliquots of 5 x 10(6) PMNL or MNC were incubated in peritoneal dialysis fluid containing 1.5% glucose or Hanks' buffer (= control) for 1-2 h at 37 degrees C. TNF alpha and LTB4 production was stimulated with Escherichia coli lipopolysaccharide (LPS) and calcium ionophore A23187, respectively. MNC incubated in buffer and LPS produced (mean +/- SD) 1,006 +/- 522 pg TNF alpha/5 x 10(6) cells; no significant amounts of TNF alpha were detectable in the presence of dialysate. An inhibition of TNF alpha release was also observed in MNC exposed to bicarbonate-buffered dialysates (pH 7.40) and 4.25% and 1.5% glucose solution with physiologic osmolality. Incubation of PMNL in Hanks' buffer followed by A23187 stimulation led to production of 29.1 +/- 19.2 ng LTB4/5 x 10(6) cells, whereas glucose-incubated cells were refractory to ionophore stimulation (less than 0.1 ng LTB4/5 x 10(6) cells). The failure of dialysate-exposed leukocytes to release inflammatory mediators in response to adequate stimuli may contribute to the impairment of cellular host defense in the setting of continuous ambulatory peritoneal dialysis.
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PMID:Leukotriene B4 and tumor necrosis factor release from leukocytes: effect of peritoneal dialysate. 165 27

The chemical structure of the saccharide portion of Vibrio parahaemolyticus serotype 012 lipopolysaccharide was studied. Using chemical degradation and modification, as well as methylation analysis in combination with GLC-MS, laser-desorption mass spectrometry and 1H-NMR and 13C-NMR spectroscopy, the carbohydrate backbone of the lipopolysaccharide was characterized as a branched decasaccharide with the following structure: (formula; see text) In the native lipopolysaccharide two additional phosphate groups are present and 3-deoxy-D-threo-hexulosonic acid and D-galacturonic acid are bound via acid-labile linkages.
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PMID:Chemical structure of the carbohydrate backbone of Vibrio parahaemolyticus serotype 012 lipopolysaccharide. 165 25

We investigated the effects of platelet-activating factor (PAF) on guinea pig peritoneal macrophages. Specific and high-affinity binding sites for PAF were detected on guinea pig peritoneal macrophages. Scatchard analysis of PAF binding revealed high affinity binding sites (7.9 x 10(4)/cell) with a dissociation constant of 2.3 x 10(-10) M. When treated with 10(-9)-10(-5) M PAF, guinea pig peritoneal macrophages released hydrogen peroxide into the medium in a time-dependent manner. The release reaction upon stimulation with 10(-5) M PAF reached a plateau within 30 min and the extent of release was twice as high as that when stimulated by N-formyl-L-methionyl-leucyl-L-phenylalanine (fMLP; 2 microM)-treated cells. Neither lysoPAF nor the PAF enantiomer was effective. PAF-induced H2O2 release was inhibited specifically by PAF antagonists, suggesting that PAF activated macrophages through binding to specific sites. Lysosomal enzyme (N-acetyl-beta-D-glucosaminidase) was released from guinea pig peritoneal macrophages upon treatment with 10(-5) M PAF for 60 min. Guinea pig peritoneal macrophages were treated with PAF for 8 hr and the conditioned medium was examined for cytokines. The medium exhibited cytocidal activity against mouse fibroblast L929 cells [tumor necrosis factor (TNF) activity], and this activity was comparable to that detected after treatment of cells with the bacterial lipopolysaccharide (LPS). Furthermore, the same conditioned medium also showed colony-stimulating factor (CSF) activity. Generation of these cytokines was stereospecific. Our findings suggest that PAF is a unique macrophage activator that potentiates both respiratory burst/lysosomal enzyme release (early-phase response) and monokine production/glucose consumption (late-phase response).
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PMID:Biological response of guinea pig peritoneal macrophages to platelet-activating factor. 166 17

Highly purified lipopolysaccharide (LPS) preparation obtained from Coxiella burnetii strain Nine Mile in phase I was used to determine the structure and monosaccharide composition of the polysaccharide component. The procedure included sodium dodecyl sulphate-polyacrylamide gel electrophoresis followed by silver staining and gel chromatographic fractionation of acetic acid-hydrolyzed LPS. Five fractions (A-E) were analysed by GLC-mass spectrometry. D-Mannose and D-glycero-D-mannoheptose were present in an appreciable amount in all polysaccharide fractions (A-D), whereas the virenose and dihydrohydroxystreptose contents varied. The highest content of both rhamnose and ribose was found in the low-molecular weight polysaccharide fraction D. The former sugar is being reported for the first time to be a LPS constituent. D-Xylose and D-glucose content varied considerably in the individual fractions and was the highest in fraction A. Glucosamine and galactosaminuronic acid were present in all polysaccharide fractions and, surprisingly, L-glycero-D-mannoheptose was also found, but its presence was limited within the certain degree of polymerisation of the polysaccharide chains. Mild acid hydrolysis of LPS resulted in a partial release of dihydrohydroxystreptose and virenose residues, which were collected and identified in fraction E. The data presented indicate a strong microheterogenity within the individual polysaccharide chains with respect to their sugar composition, size, and shape. Thus, the chemical structure of Coxiella LPS appears to represent a significant departure from the structures described for enteric LPSs.
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PMID:Evidence for the structural heterogeneity of the polysaccharide component of Coxiella burnetii strain Nine Mile lipopolysaccharide. 168 36

Polymeric material isolated from the lipopolysaccharide of the reference strain of Pseudomonas cepacia serogroup O1 consisted mainly of D-glucose and 2-amino-2-deoxy-L-glucose: rhamnose and O-acetyl groups were also present. As a result of spectroscopic and degradative studies, the disaccharide repeating-unit shown could be assigned to the major polymer present. A possible origin of the minor components is suggested. ----4)-alpha-D-Glcp-(1----3)-alpha-L-GlcpNAc-(1----.
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PMID:Structure of the putative O antigen containing 2-amino-2-deoxy-L-glucose in the reference strain for Pseudomonas cepacia serogroup O1. 169 56


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