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

Decreases in the ventilation capacity of human lungs following the inspiration of cotton dust correlates more closely with the concentration of endotoxin in the dust than with any other parameter measured thus far. A lipopolysaccharide isolated from the endotoxin of Enterobacter agglomerans, a common bacterial contaminant of cotton fiber, stimulated isolated rat macrophages to produce and release prostaglandins 6 keto-PGF1 alpha, PGF2 alpha, PGE2, PGD2, PGA2, and PGB2 and thromboxane B2. If in vivo human pulmonary macrophages respond in a similar fashion by releasing these arachidonic acid metabolites or their immediate precursors in response to stimulation by cotton dust associated lipopolysaccharides, some of the acute pulmonary changes observed in humans following inspiration of cotton dust could be caused by increased release of these biologically active compounds. Daily release of arachidonic acid metabolites at concentrations significantly above normal homeostatic levels could produce some of the pathophysiologic pulmonary changes observed in byssinotics. This paper reports the results of an experiment to quantitate arachidonic acid metabolite production following macrophage stimulation by E. agglomerans lipopolysaccharide. Procedures are described for the stimulation of macrophages by cotton dust associated lipopolysaccharide, for the separation and identification of arachidonic acid and its metabolites by high-performance liquid chromatography, and for the quantification of those products by radioisotope techniques.
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PMID:Stimulation and release of prostaglandins and thromboxane from macrophages by cotton dust associated lipopolysaccharides. 227 Aug 33

Primary rat astrocyte cultures were used to isolate a macrophage population that does not adhere to the confluent glial cells. The cells multiplied vigorously in coculture with astrocytes during the 14 d culture period, provided that functionally active lipopolysaccharide (LPS) was either absent or present in very low concentrations. Based on morphological, immunocytochemical, and pharmacological data, it was concluded that the isolated cells were microglia, the resident macrophages of the brain. The findings characterized them as a distinct cell population that shares features both of peritoneal macrophages and of astroglial cells. Like peritoneal macrophages, the isolated cells were able to phagocytize as shown by their ingestion of latex beads and uptake of L-leucyl methylester. Furthermore, they were immunocytochemically stainable by a specific monoclonal antibody (ED 1) against a macrophage-specific antigen (Dijkstra et al., 1985). They also synthesized prostaglandin E2 (PGE2) and secreted interleukin 1 (IL-1) upon stimulation with LPS. Upon stimulation with the ionophore A23187, PGD2, the predominant prostaglandin of the brain, was the major PG metabolite released by these cells. In contrast to peritoneal macrophages, microglial cells were able to multiply. Proliferation of microglial cells in coculture with astrocytes was suppressed when 2 ng LPS/ml or higher concentrations were added to astroglial culture media. These astrocyte cultures, which contained approximately 1% microglia, were used to investigate the influence of LPS on prostaglandin and IL-1 secretion in order to compare astroglial and microglial features. Increasing LPS concentrations induced increased PGE2 secretion, whereas PGD2 secretion was essentially unaffected by LPS. The critical influence of LPS contaminations in most of the commercially available animal sera used for astrocyte cultures on cellular composition in general and on metabolism of hormones and growth factors in particular is discussed.
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PMID:Lipopolysaccharide-free conditions in primary astrocyte cultures allow growth and isolation of microglial cells. 264 82

We used primary cultures of rat brain astroglial cells in order to investigate the interrelationship between PGD2 and other sleep-promoting substances such as muramyl dipeptide (MDP), lipopolysaccharide (LPS), delta-sleep-inducing peptide (DSIP), uridine, and interleukin 1 (IL-1). A large amount of PGD2 was released into the culture medium by stimulation with MDP, LPS, and IL-1 but DSIP and uridine failed to stimulate such release. These results suggest that PGD2 may be part of the series of biochemical steps involved in induction of sleep by MDP, LPS, and IL-1.
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PMID:Muramyl dipeptide-elicited production of PGD2 from astrocytes in culture. 305 5

Pulp homogenates were incubated with [14C]-arachidonic acid and the metabolites separated by thin-layer chromatography. The main products of normal pulp were 6-keto-prostaglandin (PG) F1 alpha and 12-hydroxy-eicosatetraenoic acid (12-HETE), further identified by high performance-liquid chromatography. Thromboxane (TX) B2, and PGD2, E2 and F2 alpha were also detected at less than 30 per cent of 6-keto-PGF1 alpha. When the pulp was inflamed by applying bacterial lipopolysaccharide, production of all these metabolites increased; in particular, PGE2 was increased 9.3-fold compared with normal, and 6-keto-PGF1 alpha and HETE 3.8- and 2.0-fold, respectively. An unidentified product, slightly more polar than 12-HETE, was also markedly produced by the inflamed pulp. Thus arachidonic-acid metabolites including lipoxygenase products may be involved in the development of pulpal inflammation.
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PMID:Arachidonic-acid metabolism in normal and experimentally-inflamed rat dental pulp. 312 66

Several tumor-derived murine macrophage cell lines were evaluated in vitro as cloned prototypes of tissue macrophages for their ability to metabolize arachidonic acid. Unexpectedly, two cell lines, J774A.1 and WR19M.1, rapidly converted exogenous 14C-arachidonic acid (AA) to a single major prostaglandin metabolite. The compound, PGD2, was positively identified by TLC, HPLC, and GC-MS. The enzymatic formation of the PGD2 was shown by inhibition of its formation by indomethacin and reduced formation of 14C-PGD2 from 14C-PGH2 in boiled cells. When J774A.1 cells were prelabeled with 3H-AA, cultured for 24 hours, and stimulated with lipopolysaccharide (LPS), PGD2 was again the predominant product. No other tumor derived cell lines, including several other murine macrophage lines, produced significant amounts of PGD2. Elicited and activated murine peritoneal macrophages produced only small amounts of PGD2, but resident peritoneal macrophages produced modest amounts of PGD2. Exaggerated formation of PGD2 by J774A.1 and WR19M.1 cells may be a consequence of neoplastic transformation or the clonal expansion of a minor subpopulation of normal tissue macrophages.
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PMID:Production of prostaglandin D2 by murine macrophage cell lines. 393 82

We demonstrated previously that rabbit alveolar macrophages stimulated in vitro by bacterial lipopolysaccharide (LPS) have markedly enhanced procoagulant activity (PCA), caused by increased production of a cell-associated tissue thromboplastin. The present study examined the role of arachidonic acid metabolites in modulating the expression of this PCA. Alveolar macrophages lavaged from normal rabbits were incubated in vitro with LPS, indomethacin, and purified prostaglandins, and the resultant PCA was measured. LPS stimulated a significant increase in macrophage PCA relative to unstimulated controls (p less than 0.01). Indomethacin suppressed the ability of LPS to stimulate PCA in a dose-related fashion. The addition of PGE2 or PGE1 reversed the suppressive action of indomethacin (p less than 0.01), whereas PGF2 alpha, PGD2, TXB2, and 6-keto PGF1 alpha had no such effect. PGE2 did not affect PCA unless the macrophages were also stimulated with LPS. A significant correlation (rs = 0.72, p less than 0.01) existed between the level of LPS-stimulated macrophage PCA and the corresponding amount of immunoreactive PGE2 released into the culture medium. The results of this study demonstrate that PGE is required for the LPS-mediated enhancement of rabbit alveolar macrophage-associated tissue thromboplastin and that PGE can stimulate the expression of PCA by appropriately conditioned cells.
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PMID:Prostaglandin E is required for the augmentation of procoagulant activity of LPS-stimulated rabbit alveolar macrophages. 658 Dec 28

Prostaglandins (PGs) released by cultured rat Kupffer cells in response to stimulation with lipopolysaccharide (LPS) or ethanol were extracted from culture media, separated by HPLC and measured by radioimmunoassay. LPS (0.5-5 micrograms/ml) enhanced, after a 3-4 hrs lag period, the production of PGE2 (7-10 fold by 24 hrs), thromboxane B2 (2-3 fold) and PGD2. PG 6-keto-F1 alpha, PGF2 alpha (20-50% each). This effect was not inhibited by 30 microM aspirin but was reduced by dexamethasone. Ethanol (25-85 mM) gradually increased the release of PGE2 (40-90% by 24 hrs) and other PGs (10-30%), with 30 microM aspirin eliminating this effect. When added together with LPS, ethanol potentiated the endotoxin action. We suggest that LPS causes synthesis of the inducible cyclooxygenase-2 form in Kupffer cells, whereas ethanol exerts its effect via the pre-existing cyclooxygenase-1 mainly by increasing the free arachidonic acid content.
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PMID:Secretion of prostaglandins elicited by lipopolysaccharide and ethanol in cultured rat Kupffer cells. 748 10

Endotoxin [lipopolysaccharide (LPS) 50 micrograms/mL] added to the perfusion medium increased glucose production and inhibited the glucuronidation of p-nitrophenol in perfused mouse liver both in recirculating and non-recirculating systems, while sulfation of p-nitrophenol was unchanged. The effects of endotoxin could be prevented by the addition of cyclooxygenase inhibitors, while PGD2 and PGE2 also caused a decrease in p-nitrophenol glucuronidation in perfused liver. In isolated hepatocytes endotoxin failed to affect p-nitrophenol conjugation, while PGD2 and PGE2 decreased the rate of it. Our results suggest that endotoxin inhibits glucuronidation through an intercellular communication presumably mediated by eicosanoids.
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PMID:Endotoxin inhibits glucuronidation in the liver. An effect mediated by intercellular communication. 784 Jul 84

The effect of endotoxin-derived lipopolysaccharide (LPS) and fibrinogen degradation product D (FDPD) on oxygen consumption and glycogenolysis in the perfused rat liver was investigated. 1. Infusion of LPS (100 micrograms/ml) or FDPD (7 micrograms/ml) caused a rapid stimulation of oxygen uptake by the perfused liver of 10-12 mumol/g/h. 2. LPS also caused a transient increase in glucose and lactate release into the perfusion medium from endogenous glycogen; however, FDPD was without effect. 3. Destruction of Kupffer cells by GdCl3 pretreatment blocked the effects of LPS and FDPD on oxygen uptake and glycogenolysis. Further, LPS and FDPD had no effect on oxygen consumption by isolated hepatocytes. Therefore, it is concluded that Kupffer cells are involved in the increase of hepatic oxygen consumption and carbohydrate release caused by LPS, most likely via release of PGE2 and PGD2. Since FDPD increased oxygen but not carbohydrate release, it is concluded that it acts via stimulating the release of mediators distinct from those released following LPS infusion.
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PMID:Endotoxin and fibrinogen degradation product-D have different actions on carbohydrate metabolism: role of Kupffer cells. 852 69

Prostaglandin (PG) J2 and related compounds have anti-tumor effects in vivo. To investigate possible mechanisms for this we determined effects of PGD2, PGJ2 and two PGJ2 metabolites delta 12-PGJ2 and 15-deoxy-delta 12, delta 14 PGJ2 on tumor necrosis factor-alpha (TNF-alpha) release from blood monocytes in vitro. All PGJ2 compounds stimulated TNF-alpha-release from lipopolysaccharide-activated monocytes. By contrast, the parent prostaglandin PGD2 had no stimulatory effect. We conclude that the stimulatory effect of PGJ compounds on TNF-alpha formation might contribute to the antineoplastic properties of these compounds.
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PMID:Stimulation of tumor necrosis factor-alpha release from lipopolysaccharide-activated human blood monocytes by prostaglandin J2 and metabolites of prostaglandin J2. 893 Nov 17


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