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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.01 seconds)

The mechanisms underlying the accelerated hepatic consumption of glutamine that occurs during endotoxemia were investigated in rats 12 hr after treatment with Escherichia coli lipopolysaccharide. Hepatic glutamine delivery and consumption were calculated from measurements of hepatic blood flow and blood glutamine levels. Hepatic glutaminase activity and glutamine and glutamate content were determined. Hepatocyte plasma membrane transport activity was evaluated employing isolated hepatic plasma membrane vesicles (HPMVs). Endotoxin treatment resulted in an 11-fold increase in hepatic glutamine consumption and a 2-fold increase in the delivered load of glutamine to the liver. Hepatic glutamate content doubled while glutamine content was unaffected, not withstanding a decrease in the specific activity of glutaminase. Studies employing HPMVs demonstrated that hepatic plasma membrane transport activity was unaffected by endotoxin treatment. The enhanced hepatic consumption of glutamine secondary to endotoxemia appears to be the result of both a mass-action effect and the concurrent activation of intracellular metabolism. Responses at the level of plasma membrane transport do not appear to play an active role in mediating this enhanced hepatic uptake.
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PMID:Mechanisms of increased hepatic glutamine uptake in the endotoxin-treated rat. 135 73

Role of platelet-activating factor (PAF) as a potential mediator of hepatic pathophysiology was investigated using a rat model of obstructive jaundice. Over a 1-wk course of bile duct ligation, a sixfold increase in tissue levels of PAF (1.57 +/- 0.43 ng/g vs. control 0.24 +/- 0.08 ng/g) occurred in the liver, whereas no change was observed in PAF levels in plasma. Concomitantly, endotoxin was detected in portal blood drawn from jaundiced rats, and antagonism of the putative effect of endotoxin by neomycin plus polymyxin B reduced local PAF concentrations in livers from jaundiced animals. Induction of neutropenia failed to alter the elevated hepatic PAF concentrations. Moreover, a large quantity of PAF was released spontaneously from Kupffer cells isolated from livers derived from jaundiced rats but not from endothelial cells or hepatocytes from the same animals. An in vitro study using cultured Kupffer cells from normal rats indicated that Kupffer cells secreted a significant amount of PAF in response to lipopolysaccharide challenge; pretreatment of cells with polymyxin B prevented this stimulated PAF release. Treatment of animals with either of two PAF receptor antagonists (BN 52021 and WEB 2170) partially prevented the increase in tissue levels of eicosanoids and O2-derived free radicals and partially alleviated liver injury as judged by the appearance of glutamate-pyruvate transaminase in the plasma of jaundiced rats. The present study indicates 1) that endogenous PAF may be an important signaling mediator for the hepatic inflammatory alterations associated with short-term bile duct ligation and 2) that the interaction of Kupffer cells with portal endotoxin is the mechanism by which PAF is produced locally.
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PMID:Role of platelet-activating factor in hepatic responses after bile duct ligation in rats. 144 33

The ultrastructural features and molecular components of 18 strains of Fusobacterium necrophorum biovars A, AB and B, isolated from animal and human infections, were examined by electron microscopy, multilocus enzyme electrophoresis (MEE) and by sodium dodecyl sulfate-gradient polyacrylamide gel electrophoresis (SDS-PAGE). High resolution scanning electron microscopy revealed that the strains possessed a convoluted surface pattern. Transmission electron microscopy showed that all strains possessed a cell wall structure typical of gram-negative bacteria. Bleb formation was not uncommon. Numerous extracellular materials, resembling lipopolysaccharide (LPS) fragments, surrounded cells of both human strains and biovar B animal strains. Biovar A field strains revealed capsules as stained by ruthenium red whereas a stock culture strain showed the capsule only when immunostabilized with hyperimmune serum. Starch gel electrophoresis showed all strains to possess adenyl kinase, glutamate dehydrogenases and lactate dehydrogenase; each enzyme migrated uniformly (monomorphic) among the strains and represented an electrotype. However, SDS-PAGE indicated differences in the protein profiles between all of the strains; the most distinctly different was a human isolate (FN 606). Silver staining to detect LPS showed extensive "ladder" patterns among the majority of biovar A strains but not in the animal biovar B strains. Immunoblotting of LPS with a rabbit antiserum prepared against phenol extracted LPS from a biovar A animal isolate (LA 19) suggested marked variability in the LPS antigens among the isolates studied.
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PMID:Ultrastructure and molecular characterization of Fusobacterium necrophorum biovars. 147 1

The effects of OKY-046, a selective thromboxane A2 (TXA2) synthetase inhibitor, and ONO-3708, a novel TXA2 receptor antagonist, on liver disease were investigated in mice. The liver injury was induced by either an injection of antibasic liver protein (BLP) antibody into DBA/2 mice that had been previously immunized with rabbit IgG or by an injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum (C. parvum) pretreated DDY mice. 1) In both injury models, clear elevation of glutamate transaminase (GOT and GPT) activity due to extensive liver parenchymal cell damage was observed; this was confirmed by significant histopathological changes in the liver. 2) Typical histopathological changes in the liver were submassive hepatocellular necrosis in the anti-BLP antibody-induced injury model and focal necrosis in the LPS-induced model. Inflammation and increased cell infiltration in portal connective tissue were observed in both cases. 3) Administration of OKY-046 (50 mg/kg) and ONO-3708 (0.5, 1.0 and 2.0 mg/kg) suppressed the elevation of serum GOT and GPT levels and histopathological changes in both experimental liver injury models. 4) Indomethacin inhibited the development of liver disease caused by anti-BLP antibody but not by bacterial LPS. Prostaglandin I2 inhibited the elevation of serum GOT and GPT levels and histopathological changes of the liver in the mice treated with anti-BLP antibody and showed the tendency to inhibit the development of liver injury caused by bacterial LPS.
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PMID:Effect of OKY-046 and ONO-3708 on liver injury in mice. 251 4

The role of peptide leukotrienes (p-LTs), especially LTC4 and LTD4 in liver disease, was investigated in mice experimental liver injury models. The liver injury was induced by the injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum pretreated mice. Carbon tetrachloride (CCl4)-induced liver injury in mice was used as a standard model. In both injury models, extensive liver parenchymal cell damage was observed by the elevation of glutamate transaminase (GOT and GPT) activity and confirmed by significant histopathological changes in the liver. Moreover, significant elevation of LTC4 in the liver was observed in both models 1 and 6 h after the onset of disease. Administration of AA-861, a selective 5-lipoxygenase inhibitor (0.5, 1, and 2 mg/kg) and LY-171883, a p-LT receptor antagonist (50 and 200 mg/kg) suppressed the elevation of serum GOT and GPT levels and histopathological changes in both experimental liver injury models. In addition, when authentic LTC4 or LTD4 was injected into the mouse, clear elevation of serum GOT and GPT and histopathological changes of the liver were observed. These results suggest that p-LTs play a role in the onset of liver diseases in mice.
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PMID:Role of peptide-leukotrienes in liver injury in mice. 257

Production of both alginic acid and lipopolysaccharide by a mucoid strain of Pseudomonas aeruginosa, SRM-3, was studied in a chemostat system during growth under nutrient-limiting conditions chosen to reflect the chronic growth conditions in the lungs of cystic fibrosis patients. Since mucoid strains have been shown to elaborate extracellular proteases and phospholipase C, nitrogen and phosphate limitation were selected for analysis. A modified alginate-promoting medium containing either 1 mM glutamate or 0.05 mM K2HPO4 as limiting nutrient and doubling times of 1.6 to 15.7 h were used. Under nitrogen limitation, strain SRM-3 produced 1.4 mg of uronic acid per mg (dry weight) of cells at all doubling times studied. However, phosphate limitation resulted in the synthesis of only 0.4 mg of uronic acid per mg (dry weight) of cells. The role of phosphate in alginic acid polysaccharide production was further investigated by using phosphorylcholine, a product of phospholipase C activity on phosphatidylcholine, the major lung surfactant. No only were mucoid cells capable of utilizing phosphorylcholine for growth, but a highly specific interaction occurred among phosphorylcholine, alginate, and whole cells, resulting in greatly enhanced culture viscosity. Electron micrographs showed the gradual formation of a capsule during growth on phosphorylcholine, indicating that the mucoid strain has the ability to utilize surfactant not only as a nutrient source but also for constructing a capsule with greatly enhanced adhesive properties.
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PMID:Phosphorylcholine stimulates capsule formation of phosphate-limited mucoid Pseudomonas aeruginosa. 312 46

Experimental liver injury was produced in mice by the immunological technique. The utility of these models as an immunopharmacological method was investigated. The first model was produced by the injection of anti-basic liver protein (BLP) rabbit antibody into DBA/2 mice that had been previously immunized with rabbit IgG. The second liver injury was caused by injection of anti-liver specific protein (LSP) rabbit antibody into DBA/2 mice. The third model was produced by the injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum pretreated ddY mice. In all injury models, extensive liver parenchymal cell damage was estimated by elevation of glutamate transaminase (GOT and GPT) activity. These were confirmed by histopathological studies of the liver. Typical histopathological changes in the liver from injured mice were submassive hepatocellular necrosis and infiltration of granulocytes and lymphocytes into the portal tract and sinusoid in the necrotic lesion. Administration of prednisolone and cyclophosphamide for 10 days prior to injection of eliciting antibodies or LPS suppressed the elevation of serum transaminase levels in all experimental liver injury models. Cianidanol and sylibin inhibited the elevation of GOT and GPT in anti-BLP induced liver injured mice. These evidences suggest that the above models are suitable for investigating the remedy for liver diseases.
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PMID:Liver injury model in mice for immunopharmacological study. 337 35

Cells of Pseudomonas aeruginosa 015 were grown in basal medium with isobutyrate, DL-2-methylbutyrate, isovalerate, L-valine, L-isoleucine, L-leucine, D-glucose, or L-glutamate as the carbon source. Their resultant susceptibility to polymyxin B varied from a minimal inhibitory concentration of 2 U of polymyxin per ml for isobutyrate-grown cells to 975 U/ml for L-glutamate-grown cells. Cell envelopes from cells grown with each carbon source were compared with cell envelopes from cells grown in Mueller-Hinton broth as to their content of total protein, carbohydrate, and 2-keto-3-deoxyoctonate and as to their protein composition as determined by slab polyacrylamide gel electrophoresis. No pattern of cell envelope content of total protein, carbohydrate, 2-keto-3-deoxyoctonate, or outer membrane protein concentrations could be correlated with the degree of resistance to polymyxin. In these cells increased resistance to polymyxin was not associated with the loss of outer membrane proteins and lipopolysaccharide by the cell envelope.
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PMID:Effects of carbon sources on chemical composition of cell envelopes of Pseudomonas aeruginosa in association with polymyxin resistance. 624 93

We investigated whether administration of monosodium 1-glutamate (MSG) to neonatal rats would disrupt immune responses in intact and orchidectomized adult male rats. Neonatal male rats were treated with saline or MSG which causes severe endocrine abnormalities. Half of each group of animals were orchidectomized as adults and killed one week later along with intact rats. MSG treatment resulted in suppressed serum LH levels in intact rats. Thymus weight and spleen cellularity in intact animals were not affected by MSG treatment, but thymus weight increased within one week after orchidectomy in both saline- and MSG-treated groups. In intact rats, lymphocyte stimulation by the T cell specific mitogens (concanavalin A or phytohemagglutinin) or the B cell specific mitogen (lipopolysaccharide) was unaffected by prior treatment with MSG. However, MSG treatment blocked the decrease attributable to orchidectomy in concanavalin A and phytohemagglutinin stimulation of lymphocyte blastogenesis. The results suggest that administration of MSG to neonatal male rats can alter some immune responses in the adult animal.
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PMID:A decrease in thymus-mediated immune responses as a result of treatment of neonatal rats with glutamate. 643 29

Escherichia coli O127:B8 lipopolysaccharide (LPS) inhibited oxygen consumption by isolated mouse liver mitochondria at 10 micrograms of LPS per mg of protein when glutamate + malate was the substrate and adenosine 5'-diphosphate had been added (state 3 respiration), but had little effect when adenosine 5'-diphosphate was not added (state 4 respiration). LPS stimulated state 4 respiration at 10 micrograms/mg of mitochondrial protein when succinate was the substrate but had little effect on state 3 respiration. Lipid A from Shigella sonnei at 2 micrograms/mg of mitochondrial protein also stimulated state 4 respiration but did not affect state 3 respiration with succinate as the substrate. Lipid A, unlike LPS, caused a decrease in the adenosine 5'-diphosphate/O ratio. LPS at 100 micrograms/mg of mitochondrial protein impaired the reduction of cytochromes aa3, c, and b when succinate was the substrate but not when reduced nicotinamide dinucleotide, dithionite, or glutamate was the substrate.
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PMID:Action of bacterial lipopolysaccharide on the respiration of mouse liver mitochondria. 698 63


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