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

The phagocytic, oxygen free radical generating and cytotoxic activities of macrophages from C57BL/6J mice fed either a normal or an atherogenic high-fat diet have been investigated. Phagocytosis of aggregated low density lipoprotein (LDL) was only slightly inhibited by the high-fat diet although phorbol myristate acetate (PMA)-induced hydrogen peroxide (H2O2) and superoxide anion (O2-) production was significantly reduced. Activation of tumoricidal activity against L929 target cells by lipopolysaccharide (LPS) or lymphocyte-derived macrophage-activating factor (MAF), but not N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP), was also significantly reduced in macrophages from mice fed the high-fat diet. These results indicate that an atherogenic diet is capable of significantly affecting the responsiveness of macrophages to a number of stimulatory agents which act via specific membrane receptors.
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PMID:The effect of a high-fat diet on murine macrophage activity. 205 Apr 36

Using cultured human umbilical cord vein endothelial cells and human blood neutrophils, the interaction between neutrophils and endothelial cells, in vitro, was studied. The aim of the study was to examine whether a respiratory burst stimulation by neutrophils would be observed by neutrophil/endothelial cell interaction and whether the respiratory burst stimulation of neutrophils by endothelial cells could be enhanced by lipopolysaccharide stimulation of neutrophils. The second aim was whether such an effect, or secretion of elastase, could cause an endothelial cell damage in vitro. Chemiluminescence as an indicator of oxygen-derived metabolites produced by neutrophils, elastase release by neutrophils, and endothelial cell damage, based on 111 In-oxine release from labelled endothelial cells, were measured simultaneously. The present investigation demonstrates that neutrophils can be directly stimulated by endothelial cells. A further amplification of this process following lipopolysaccharide priming up to 10 ng/ml blood could be demonstrated. A slight endothelial cell damage occurs following neutrophil stimulation, although elastase secretion does not increase during interaction between neutrophils and endothelial cells. These results raise the possibility that oxygen-derived metabolites rather than elastase contribute to an endothelial cell damage which might occur in conditions such as endotoxin-induced adult respiratory distress syndrome.
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PMID:Simultaneous measurement of endothelial cell damage, elastase release and chemiluminescence response during interaction between polymorphonuclear leukocytes and endothelial cells. 205 64

Hydrogen peroxide and oxygen radicals are agents commonly produced during inflammatory processes. In this study, we show that micromolar concentrations of H2O2 can induce the expression and replication of HIV-1 in a human T cell line. The effect is mediated by the NF-kappa B transcription factor which is potently and rapidly activated by an H2O2 treatment of cells from its inactive cytoplasmic form. N-acetyl-L-cysteine (NAC), a well characterized antioxidant which counteracts the effects of reactive oxygen intermediates (ROI) in living cells, prevented the activation of NF-kappa B by H2O2. NAC and other thiol compounds also blocked the activation of NF-kappa B by cycloheximide, double-stranded RNA, calcium ionophore, TNF-alpha, active phorbol ester, interleukin-1, lipopolysaccharide and lectin. This suggests that diverse agents thought to activate NF-kappa B by distinct intracellular pathways might all act through a common mechanism involving the synthesis of ROI. ROI appear to serve as messengers mediating directly or indirectly the release of the inhibitory subunit I kappa B from NF-kappa B.
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PMID:Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1. 206 63

Intrajugular injection of a purified E. coli lipopolysaccharide induced a biphasic fever in sheep after a latent period of 12 to 20 min. The changes in the blood flow from the liver and from the viscera drained by the portal vein were: (a) in the latent period, decreases in total hepatic blood flow (THF) due to decreased portal venous blood flow (PVF); (b) during the first febrile phase, increases in THF due to increased hepatic arterial blood flow and, (c) in the second febrile phase, decreases in THF due to decreased PVF. Although there were large variations in the oxygen supply to the viscera drained by the portal vein and to the liver, there were relatively small or no changes in their oxygen consumption.
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PMID:The effects of experimentally induced fever on the estimated blood flow to and oxygen utilization by the liver and the viscera drained by the portal vein in sheep. 206 99

In an attempt to elucidate the effect of lipoxygenase inhibitors on hepatic injury, we investigated D-galactosamine (GalN)-treated C57BL/6 mice receiving an intravenous (i.v.) injection of lipopolysaccharide (LPS)-activated autologous spleen cells. As compared with control spleen cells, the number of monocytes in the spleen cells isolated from LPS-treated mice and their oxidative free radical production increased markedly. Oxygen radical production by the dish-adherent cells (macrophage-rich population) was enhanced a further 4-fold. Although hepatotoxicity was not demonstrated in mice treated with 20 mg GalN alone, marked hepatic injury was found in the GalN-treated mice with a supplementation of LPS-activated spleen cells. The dish-adherent cells aggravated this hepatic injury, in contrast to minor hepatotoxicity by the nonadherent cells. Oxygen radical production by LPS-activated spleen cells was markedly reduced by the lipoxygenase inhibitors (azelastine, ketotifen and AA861). Hepatotoxicity was scarcely detected in the GalN-treated mice with a supplementation of the LPS-activated spleen cells which had been previously treated with lipoxygenase inhibitors. From these results, LPS-activated spleen macrophages contributed to hepatic injury induced by GalN, and lipoxygenase inhibitors which reduced oxygen radical production by the activated cells, protected against macrophage-induced hepatic injury in mice.
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PMID:Leukotriene inhibitors modulate hepatic injury induced by lipopolysaccharide-activated macrophages. 210 47

The enzyme xanthine oxidase participates in the pathogenesis of tissue ischemia-reperfusion injury by depleting purine pools and generating toxic oxygen metabolites. The role of xanthine oxidase in inflammatory cell populations has not been defined. We examined the level of xanthine oxidase activity expressed by murine leukocytes both in the resting state, and after in vivo and in vitro exposure to inflammatory stimuli. The contribution of xanthine oxidase to inflammation may vary among tissue compartments, so leukocytes harvested from several tissues were studied. Resident murine peritoneal macrophages consistently expressed xanthine oxidase activity (291 +/- 55 microIU/10(6) cells). Thioglycolate-elicited peritoneal macrophages contained similar levels of xanthine oxidase activity (265 +/- 42 microIU/10(6) cells). By contrast, resident murine alveolar macrophages expressed one tenth the xanthine oxidase activity (24 +/- 4 microIU/10(6) cells). Xanthine oxidase activity was also consistently found in murine peritoneal neutrophils (127 +/- 28 microIU/10(6) cells) but not in splenic lymphocytes. In vitro studies were performed to determine whether xanthine oxidase activity of resident peritoneal macrophages could be modulated by exogenous stimuli relevant to the pathogenesis of inflammation. Lipopolysaccharide caused a 62% +/- 9% reduction in cellular xanthine oxidase activity (p less than 0.02). Interferon-gamma alone had no effect on xanthine oxidase activity; however, interferon-gamma and lipopolysaccharide together caused a striking reduction in cellular xanthine oxidase activity, reaching 25% +/- 2% of unstimulated control cells (p less than 0.001). We conclude that murine macrophages and neutrophils are potentially important sources of xanthine oxidase activity in inflamed tissues. In addition, the activity of xanthine oxidase in macrophages is tissue specific and is modulated in vitro by proinflammatory stimuli.
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PMID:Expression of xanthine oxidase activity by murine leukocytes. 211 59

The pharmacologic modulation of the effect of platelet-activating factor (PAF) on the interleukin-1 (IL-1) activity present in the supernatants from lipopolysaccharide (LPS)-stimulated macrophages was investigated. Rat spleen macrophages were isolated by centrifugation on a Ficoll-Hypaque gradient followed by adherence on plastic petri dishes for 60 min at 37 degrees C under a 5% CO2/95% air atmosphere. The IL-1 content in the cell-free supernatants was assessed using the mouse thymocyte proliferation assay. Preincubation of macrophages for 10 min with 10 fM PAF prior to stimulation with 20 micrograms/ml LPS for 24 h markedly increased the IL-1 activity present in the supernatants from macrophages whereas no direct effect of PAF was noted. Although they had no direct effect, addition of L-651,392 (10 microM), a lipoxygenase inhibitor, or the oxygen-derived free radical scavenger mannitol (10 microM) during the 10-min preincubation period with PAF reversed by 105.0% and 79.9%, respectively, the action of the autacoid on IL-1 activity. Pertussis toxin (PT, 1 microgram/ml) decreased by 30% the LPS-induced IL-1 activity. Association of PT with PAF suppressed the enhancing effect of 10 fM PAF on the IL-1 activity present in the supernatants from LPS-stimulated macrophages. Thus, the enhancing effect of PAF on IL-1 release appears to be due to the production of lipoxygenase metabolites, leading to superoxide production and alterations of cAMP levels.
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PMID:Modulation of the priming effects of platelet-activating factor on the release of interleukin-1 from lipopolysaccharide-stimulated rat spleen macrophages. 213 88

Human neutrophils were primed by exudation or pretreatment with a synthetic diacylglycerol (diC10), the Ca2+ ionophore ionomycin or lipopolysaccharide (LPS). Compared to control cells, these primed cells showed a significantly decreased O2-/H2O2 ratio when stimulated with formylmethionyl-leucyl-phenylalanine (FMLP). This shift indicates a comparative (and net) increased H2O2 detection in the extracellular medium and can not be explained by a dose-dependent impairment in either O2- or H2O2 detecting capacity. An altered H2O2 degenerating capacity was not observed in the primed cells. We propose that priming enhances the capacity to divalently reduce oxygen and thereby directly produce H2O2.
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PMID:Altered O2-/H2O2 production ratio by in vitro and in vivo primed human neutrophils. 215 35

Reactive oxygen species (ROS) have generated increasing interest for their possible role in a wide variety of diseases. Interferon-gamma (IFN-gamma), a potent immunoregulatory lymphokine, is likely involved in control of ROS metabolism. In this study, the superoxide release of cultured human peripheral blood monocytes (PBM) after exposure to IFN-gamma and lipopolysaccharide (LPS) was examined. Compared with controls, adherent monocytes cultured with 80 units of IFN-gamma for 48 hours demonstrated fourfold increased spontaneous and twofold increased PMA stimulated release of superoxide anion. In addition, the enhanced superoxide release was both dose and time dependent. Further experiments showed that bacterial LPS in concentrations as low as 4 ng/mL markedly reduced monocyte superoxide release and abrogated the enhancing effects of IFN-gamma.
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PMID:Modulation of human peripheral blood monocyte superoxide release by interferon-gamma and lipopolysaccharide. 216 40

It is known that lipopolysaccharides (endotoxin) prime neutrophils for oxygen radical production. Monophosphoryl lipid A is a nontoxic derivative of lipid A that protects against lethal endotoxemia. We examined the effects of Salmonella minnesota monophosphoryl lipid A on S. minnesota lipopolysaccharide-induced priming of neutrophil superoxide anion generation. Human neutrophils were preincubated with and without either lipopolysaccharide or monophosphoryl lipid A before stimulation with 10(-5) formyl-norleucyl-leucyl-phenylalanine. Neutrophil priming reached a plateau at a concentration of 100 ng/ml of lipopolysaccharide, where superoxide anion generation increased from 10.1 +/- 0.8 to 25.2 +/- 1.7 nmol superoxide anions/10(6) neutrophils/10 min (p less than 0.01). In contrast, monophosphoryl lipid A did not exhibit any priming activity. Monophosphoryl lipid A also exhibited a time-dependent inhibitory effect on lipopolysaccharide-induced priming of neutrophils, which was maximal when monophosphoryl lipid A was added 15 minutes before lipopolysaccharide. Preincubation with monophosphoryl lipid A induced a dose-dependent inhibition of neutrophil priming by 1000 ng/ml lipopolysaccharide. Neutrophil superoxide anion generation decreased by 47% from 19.0 +/- 0.6 to 10.0 +/- 0.7 nmol superoxide anions/10(6) neutrophils/10 min by 2000 ng/ml monophosphoryl lipid A (p less than 0.01). These data indicate that monophosphoryl lipid A does not enhance neutrophil superoxide generation in response to formyl-norleucyl-leucyl-phenylalanine. Monophosphoryl lipid A also inhibits lipopolysaccharide-induced priming in a dose-dependent manner that may reflect blocking of lipopolysaccharide by monophosphoryl lipid A at cellular binding sites.
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PMID:Monophosphoryl lipid A inhibits neutrophil priming by lipopolysaccharide. 216 64


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