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)

Cloning procedures were used to study B lymphocytes and progenitors of granulocytes and macrophages in NZB mice. Numbers of B cells that were detected in sheep erythrocyte-containing semisolid cultures were only slightly elevated in NZB tissues, and these were normally sensitive to inhibition by anti-mu or anti-delta antibodies or prostaglandin E. However, NZB mice rapidly developed large numbers of B cells that could be cloned in the presence of lipopolysaccharide, and these included unusual anti-mu resistant cells. Numbers of myeloid precursors in NZB bone marrow that were responsive to colony-stimulating activity in L-cell conditioned medium or endotoxin serum were at least normal, but at all ages granulocyte-macrophage precursors were poor responders in cultures stimulated by WEHI-3 cell conditioned medium. Almost no colonies were elicited in NZB cultures with a colony-stimulating activity moiety from WEHI-3 cells. Prostaglandin sensitivity of myeloid precursors from NZB and CBA mice was also different. Codominant genetic control of these abnormalities was suggested by their partial expression in F1 hybrid NZB X CBA and NZB X NZW mice. NZB mice expressed an unexpected IgD allotype allele.
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PMID:Abnormalities in clonable B lymphocytes and myeloid progenitors in autoimmune NZB mice. 11 1

Prostaglandin H synthase is a key enzyme in the formation of prostaglandins and thromboxane from arachidonic acid. The recent cloning of a second prostaglandin H synthase gene, prostaglandin H synthase-2, which is distinct from the classic prostaglandin H synthase-1 gene, may dramatically alter our concept of how cells regulate prostanoid formation. We have recently shown that the enhanced production of prostanoids by lipopolysaccharide-primed alveolar macrophages involves the induction of a novel prostaglandin H synthase (J. Biol. Chem., (1992), 267, 14547-14550). We report here that the novel PGH synthase induced by lipopolysaccharide in alveolar macrophages is prostaglandin H synthase-2.
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PMID:Lipopolysaccharide induces prostaglandin H synthase-2 in alveolar macrophages. 138 14

Prostaglandin-E2 (PGE2) and interleukin-1 (IL-1) production from plastic-adherent peripheral blood mononuclear cells stimulated in vitro by bacterial lipopolysaccharide, serum and urinary glucocorticoid levels and the circadian rhythm of serum cortisol levels were studied for better understanding of the immunological and physiological changes produced by systemic chemotherapy in cancer patients. In one responded patient out of four, PGE2 production decreased and IL-1 production increased, whereas the serum cortisol level decreased and the urinary 17-KS excretion level increased. The circadian rhythm of the serum cortisol level was evaluated three times a day, at 7 A.M., 2 P.M. and 10 P.M. Healthy volunteers showed a peak level at 7 A.M. which decreased gradually towards evening and reached to the lowest level at 10 P.M. In contrast, cancer patients showed three additional patterns. These patterns were classified as follows, Type N showed a maximal level at 7 A.M. and minimal level at 10 P.M. as same as in healthy subjects. Type V showed a minimal level at 2 P.M. while type A showed a maximal level at this time. In type F the serum cortisol level was no greater than 1.0 micrograms/dl at any of the three time points. We examined circadian rhythm in four cancer patients treated with systemic chemotherapy. In one PR case, the circadian rhythm shifted from type V to N after the first course of therapy, then changed to type F after subsequent and another courses of the therapy. In another PR case, type N persisted during and after therapy. One MR case shifted from type A to type N. In contrast, one PD case shifted from type N to A. There results suggest that normalization of the circadian rhythm of serum cortisol was associated with the improvement in host body condition achieved by chemotherapy and that systemic chemotherapy modified the immunological and physiological state of cancer patients, as defined above. This may eventually be beneficial for patients.
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PMID:[Prostaglandin-E2 (PGE2) and interleukin-1 (IL-1) production from plastic-adherent peripheral blood mononuclear cells, and serum and urinary glucocorticoid levels in cancer patients treated with systemic chemotherapy--with special reference to circadian rhythm of serum cortisol levels in cancer]. 232 78

The cell walls of gram-negative bacteria contain several biologically active components, including lipopolysaccharide (LPS), lipoprotein, and protein 1. The effects of these individual components and a synthetic analog of lipoprotein, TPP, on several activation parameters of glomerular mesangial cells (MC) were examined. Prostaglandin secretion, synthesis of the autogrowth factor, mesangial interleukin-1 (IL-1), and new synthesis of cellular proteins were assessed as markers of MC activation. All bacterial cell wall components evaluated were active in varying degrees as stimulants of prostaglandin secretion. In general, PGE was the predominant product. TPP and protein 1 also induced substantial secretion of thromboxane. Each cell-wall component was effective in stimulating mesangial IL-1 secretion. The activation of MC was associated with the enhanced synthesis of many cellular proteins in addition to IL-1. Stimulation by these bacterial components was dependent on the state of the mesangial cell cycle, because nonproliferating cells did not respond to these factors. Activation of MC by gram-negative bacterial cell wall components, with release of vasoactive prostaglandins and peptide mitogens, may be responsible for some of the glomerular hemodynamic alterations and cellular proliferative events associated with sepsis or chronic bacterial infection.
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PMID:Activation of glomerular mesangial cells by gram-negative bacterial cell wall components. 305 3

Prostaglandin-releasing, adrenocortical, febrile and miotic responses to endotoxin (ET) (E. coli lipopolysaccharide; 0.25 microgram kg-1) were studied in goats with and without prolonged dexamethasone influence. The i.v. injection of ET induced a three-fold peak elevation in plasma 15-ketodihydro-PGF2 alpha at 1.5 h post-injection, that is, between the first and second phase of the temperature elevation. During the latter phase, the plasma concentration of this primary PGF 2 alpha metabolite gradually returned to basal level, which implies that the second phase of ET fever is not PG dependent. The PG response exhibited a similar pattern, but was less pronounced in the dexamethasone-ET experiments, where the duration of maximum temperature elevation and of the miosis became shortened by about 20 min, and the typical biphasic pattern of ET fever was no longer seen. The ET-induced rise in plasma aldosterone concentration was completely blocked by dexamethasone. The corresponding rise in plasma cortisol concentration was prevented for 2 h, but was later only partially inhibited in spite of the repeated dexamethasone treatment.
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PMID:Endotoxin-induced prostaglandin (PGF2 alpha) biosynthesis, fever and miosis in dexamethasone-treated goats. 331 53

Macrophages are a prominent resident cell type in the interstitial tissue of the testis in several mammalian species. This presence in an immunologically-privileged site prompted an investigation of their ability to initiate and regulate lymphocyte proliferation in vitro. Isolated rat peripheral blood lymphocytes (PBL) were cultured either directly with isolated rat testicular (Tm) or peritoneal (Pm) macrophages or with the conditioned medium from cultures of these cells (Ts or Ps). The presence of Tm and Ts reduced the proliferative response of PBL to 65% +/- 3% and 65% +/- 4% of that observed in the control cultures. Stimulation of the Tm with lipopolysaccharide (LPS) did not significantly alter this effect. Dialysis of Ts (to remove molecules < 14,000 MW) before addition to PBL cultures did significantly reduce the amount of inhibition, with PBL proliferation reaching 93% +/- 4% of the control. LPS in conjunction with indomethacin (IDM) or interferon gamma (IFN gamma) induced PBL proliferation at levels comparable to or significantly greater than those of the controls (104% +/- 4% and 113% +/- 6%, respectively). The collective addition of IDM, IFN gamma and LPS to Tm cultures increased PBL proliferation over control levels (119% +/- 5% for Ts and 133% +/- 6% for Tm). Prostaglandin levels in macrophage-conditioned medium were measured by specific radioimmunoassay and were significantly greater in Ts (13.1 +/- 0.4 ng/ml PGE2 and 16.8 +/- 0.6 ng/ml PGF2 alpha) than in Ps (both below the assay minimum sensitivities). The results indicate that the rat testicular macrophages produce high basal levels of prostaglandin E2 and F2 alpha. These products appear largely responsible for the inhibition by these cells of mitogen-induced PBL proliferation in vitro, and may contribute to both the immune-privileged status and the normal physiology of the rodent testis.
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PMID:Indomethacin blocks the immunosuppressive activity of rat testicular macrophages cultured in vitro. 747 30

Kupffer cells are the largest population of fixed tissue macrophages in the body and produce a number of mediators that are involved in host defense. These mediators include cytokines such as tumor necrosis factor-alpha and interleukin-1, prostaglandins, oxygen radicals, and nitric oxide. Prostaglandins are produced by adjacent endothelial cells in addition to Kupffer cells and regulate a number of cellular functions in a wide array of cells, but their role in nitric oxide synthesis is controversial. We studied the role of prostaglandins in regulating lipopolysaccharide (LPS)-induced nitric oxide synthesis in cultured rat Kupffer cells. Prostaglandin E2 (PGE2) inhibited Kupffer cell nitric oxide synthesis in a dose-dependent fashion in both 24- and 48-hr cultures. The effect of PGE2 persisted at low and high LPS concentrations. Prostaglandin analogues as well as other prostanoids also inhibited Kupffer cell nitric oxide synthesis. These data show that exogenous prostaglandins suppress Kupffer cell nitric oxide synthesis and may represent an important endogenous regulator of nitric oxide production.
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PMID:Prostanoids inhibit Kupffer cell nitric oxide synthesis. 779 38

Prostaglandin synthesis represents one means by which macrophages modulate inflammation. The initial enzyme in the metabolism of arachidonic acid to prostaglandins is cyclooxygenase (COX). Both constitutive (COX-1) and inducible (COX-2) isoforms are recognized. We previously showed that COX activity of rat peritoneal macrophages (PM) exceeds that of alveolar macrophages (AM). In this study, we correlated the steady-state levels of COX-1 and COX-2 proteins with COX activity in resident AM and PM. Freshly obtained AM contained lower levels of COX-1 than did fresh PM. Neither contained substantial amounts of COX-2 in the basal state, but both cell types demonstrated induction when cultured with lipopolysaccharide; once again, COX-2 levels in PM exceeded those in AM. Despite COX-2 induction under these circumstances, its contribution to prostaglandin production appeared to be modest. We conclude that, although both isoforms of COX are expressed in rat AM and PM, COX-1 is responsible for the majority of enzyme activity in both the basal and stimulated states. The lesser prostaglandin synthetic capacity of AM than of PM appears to be the consequence of lower steady-state levels of both COX proteins.
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PMID:Expression and role of cyclooxygenase isoforms in alveolar and peritoneal macrophages. 786 49

Prostaglandin endoperoxide synthase (PHS) catalyzes the committed step in the biosynthesis of prostaglandins and thromboxane. We recently observed dissociation of PHS activity and enzyme mass measured in an immunoassay of endothelial cells exposed to tumor necrosis factor. These data and observations by others suggested that endothelial cells express an alternate PHS. We now report the molecular cloning of human PHS type II from an endothelial cell cDNA library. The protein encoded by this cDNA shares 61% identity with the human PHS I. Southern analysis demonstrated a single copy of PHS II and we found a polymorphism in approximately 5% of the population. PHS II mapped to chromosome 1, in contrast to PHS I, which is on chromosome 9. The PHS II cDNA hybridized strongly to a 4.3-kilobase (kb) message from endothelial cells. Stimulation of the cells with tumor necrosis factor, phorbol 12-myristate 13-acetate, lipopolysaccharide, or interleukin-1 increased mRNA levels for PHS II, and this change correlated well with increased prostacyclin biosynthesis. Cycloheximide induced PHS II mRNA without a corresponding activity increase demonstrating that translation of the 4.3-kb message is required for increased prostacyclin biosynthesis. We conclude that expression of PHS II may have important pathophysiological effects in the vasculature.
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PMID:Molecular cloning of human prostaglandin endoperoxide synthase type II and demonstration of expression in response to cytokines. 847 46

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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