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)

Macrophage-mediated antitumor activity is believed to be regulated by E-type prostaglandins released by target cells or even by macrophages themselves. In these studies we showed that a subcutaneous injection of polyacrylamide beads (Biogel P100), induced in mice, a population of immature macrophages which became fully cytostatic to syngeneic P815 mastocytoma when pulsed in vitro with lipopolysaccharide (LPS). Blockade of prostaglandin synthesis by indomethacin prevented LPS effect and led to a substantial resumption of target growth. Addition of PGE2 did not reverse the indomethacin effect but inhibited macrophage-mediated cytostatic activity. These findings suggest that acquisition of cytostatic properties by macrophages is, at a certain stage of their maturation, under the control of both PGE2 and another endogenously produced eicosanoid.
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PMID:Development of antitumor activity in LPS-stimulated mouse granuloma macrophages. Regulation by eicosanoids. 308 25

The release of ornithine by macrophages and its correlation with their immunogenicity after treatment with various macrophage-stimulating substances were analyzed. Pristane-elicited peritoneal macrophages (PM) were found to express strong arginase activity and to release L-ornithine into the extracellular space. This activity is strongly reduced within 3 hr after treatment with tetradecanoylphorbol acetate (TPA) but not with lipopolysaccharide (LPS). Resident PM usually express little arginase activity, but this activity is markedly augmented within 24 or 48 hr after treatment with LPS. The release of ornithine by peritoneal cells (PC) (60 to 90% macrophages) was found to be correlated with their immunogenicity as determined by the in vivo immunization for a subsequent in vitro secondary cytotoxic response against minor H antigens. The immunogenicity of pristane-elicited PC is markedly stronger than that of resident PC or TPA-treated, pristane-elicited PC. Moreover, the immunogenicity of the resident PC and TPA-treated elicited PC is substantially augmented by the simultaneous injection of ornithine, whereas the immunogenicity of the untreated elicited PC is not further augmented by exogenous ornithine, indicating that the endogenous production of ornithine by the stimulating cells had a strong influence on the resulting immune response. Injection of glutathione into pristane-treated mice also reduces the ornithine production and immunogenicity of the resulting peritoneal exudate cells. The immunogenicity in this case is at least partly reconstituted by application of exogenous ornithine. Our experiments revealed no correlation between the production of ornithine and prostaglandin E2. Prostaglandin E2 production of resident and pristane-elicited PC is not markedly different and is in either case strongly augmented by TPA. Elicited or resident PM which have been incubated for several days in culture release practically no ornithine; but ornithine production can be induced again by incubation for 24 hr with LPS and to some extent also with interferon-gamma.
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PMID:Correlation of immunogenicity and production of ornithine by peritoneal macrophages. 311 Feb 88

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

Stimulated monocytes produce prostaglandins (PGE2) in response to lipopolysaccharide (LPS), Muramyl dipeptide (MDP) or Interleukin-1 (IL-1). This response could be modulated in different ways by Interferon-gamma (IFN-gamma). This lymphokine, known to potentiate IL-1 production by LPS- or MDP-stimulated monocytes, suppressed different Il-1 activities such as PGE2 release by the same cells. By contrast, an impairement of suppression by IFN-gamma was evidenced in rIL-1 beta-induced PGE2 release from human dermal fibroblasts. Salmon calcitonin (sCT), another inhibitor of IL-1-induced bone resorption, was able to prime monocytes to potentiate PGE2 elaboration by LPS, but failed to modulate PGE2 liberation from either rIL-1 beta-stimulated monocytes or fibroblasts.
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PMID:Opposite effect of Interferon-gamma on PGE2 release from Interleukin-1-stimulated human monocytes or fibroblasts. 314 68

Evidence is presented that upon stimulation with endotoxin (lipopolysaccharide, LPS), Kupffer cells, the body's largest pool of sessile macrophages, synthesize and liberate a factor whose immunological, cytotoxic and chemical properties are those described for tumor necrosis factor (TNF)-alpha. Hepatocytes and sinusoidal endothelial cells do not produce detectable amounts of this protein. Ten nanograms of LPS per ml medium are sufficient to stimulate a substantial release of this mediator. Recombinant interferon-gamma (rIFN gamma) per se is a poor inducer of TNF release. Costimulation with endotoxin and rIFN gamma shows only a slight increment in the release of this cytotoxic factor, relative to LPS alone. Exposure of Kupffer cells to the Ca2+ ionophore A23187 or to elicitors of the oxidative burst and superoxide production, e.g. zymosan or phorbol 12-myristate 13-acetate, stimulates only a fraction (20%) of the TNF release seen after endotoxin challenge. Prostaglandin E2, the synthesis of which is strongly enhanced after challenge of rat Kupffer cells with LPS, suppresses the release of TNF by these cells. This autoregulatory mechanism may explain the kinetics of TNF production by stimulated Kupffer cells. Dexamethasone is another important mediator capable of reducing the LPS-elicited TNF formation. An effect of the glucocorticoid hormone can still be provoked if it is added simultaneously with or shortly after LPS. This rapid action requires a mechanism that is different from the time-consuming one leading to the inhibition of prostaglandin synthesis in Kupffer cells.
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PMID:The release of tumor necrosis factor from endotoxin-stimulated rat Kupffer cells is regulated by prostaglandin E2 and dexamethasone. 314 53

Tumor necrosis factor-alpha (TNF) is a macrophage-derived peptide that is known to be an important mediator in various physiologic and immunologic events. Although the effector function of TNF has received recent attention, there is relatively little information regarding factors that regulate TNF expression. Highly Ia-positive murine peritoneal macrophages obtained via complete Freund's adjuvant elicitation were challenged with lipopolysaccharide (LPS) and assessed for the production and regulation of TNF at the cellular and molecular levels. In response to 1 microgram/ml LPS, the kinetics of functionally active TNF reached a maximum at approximately 3-4 h. The plateau in TNF levels was concomitant with an accelerated increase in prostaglandin E2 production. The addition of exogenous PGE2 demonstrated a dose-dependent reduction in LPS-induced TNF activity at the cellular level, as well as a significant reduction in TNF mRNA accumulation as assessed by Northern blot and in situ hybridization analysis. The reduction in LPS-stimulated mRNA accumulation by PGE2 was shown to occur at least at the level of transcription, since nuclear run-off analysis showed a specific reduction in TNF transcripts. These studies demonstrate that PGE2 can regulate macrophage-derived TNF gene expression.
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PMID:Prostaglandin E2 regulates macrophage-derived tumor necrosis factor gene expression. 316 31

To distinguish pattern differences in experimentally induced fevers, we investigated febrile responses induced by intravenous (IV), intracerebroventricular (ICV), and intra-preoptic/anterior hypothalamic (POA) administration of bacterial endotoxin (lipopolysaccharide, LPS), endogenous pyrogen (EP), human recombinant interleukin-1 alpha (IL-1), and prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha). Intravenous LPS, EP, or IL-1 in high concentrations caused biphasic fever. In low concentrations, they induced only the first phase of fever. Latency to onset and time to first peak of fever induced by IV injection of LPS or EP were almost the same as those after ICV or POA injection of PGE2. Fever induced by ICV or POA administration of LPS, EP, IL-1, or PGF2 alpha had a long latency to onset and a prolonged time course. There were significant differences among the latencies to fever onset exhibited by groups that received ICV or POA injections of LPS, EP, or PGF2 alpha and by groups given IV injections of LPS or EP and ICV or POA injections of PGE2. Present observations indicate different patterns of fever produced by several kinds of pyrogens when given by various routes. These results permit us to consider the possibility that there are several mediators or multiprocesses underlying the pathogenesis of fever.
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PMID:Pattern differences in experimental fevers induced by endotoxin, endogenous pyrogen, and prostaglandins. 325 78

In order to study the possible role of alveolar macrophages (AMs) in the development of local immune responses, we compared interleukin-1 (IL-1) production by peripheral blood monocytes and AMs from 17 allergic asthmatics and 32 controls. When stimulated by lipopolysaccharide, alveolar macrophages and blood monocytes from controls released IL-1 (127 +/- 74.6 and 178.8 +/- 120 IL-1 units/ml, respectively) in the same amounts as AMs and blood monocytes from allergic asthmatics (148 +/- 47.5 and 160.5 +/- 78.3 IL-1 units/ml, respectively). After stimulation by anti-IgE or the specific allergen, asthmatic blood monocytes released IL-1-like activity (71.8 +/- 46.4 and 45.4 +/- 25.9 IL-1 units/ml, respectively). In contrast, asthmatic AM supernatants contained no detectable IL-1-like activity after stimulation by allergen or anti-IgE. The same pattern was observed with monocytes and AMs from controls after passive cell sensitization with 20% of IgE-rich serum. In a second step, the effect of supernatants of IgE-dependent stimulated AMs was tested on thymocyte proliferation induced by a purified IL-1, permitting the demonstration of an IL-1 inhibitory factor released by the AMs while these supernatants didn't modify the IL-2-dependent proliferation of a CTL-L line. The use of indomethacin and assessment of PGE2 levels in AM supernatants made it possible to discard the role of prostaglandins in this inhibitory effect. Moreover this activity, which is resistant to heat and trypsin treatment, has a molecular mass between 40 and 50 kD and did not correspond to serum proteases, alpha-1-antiproteinase, and arginase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Production of an interleukin-1 inhibitory factor by human alveolar macrophages from normals and allergic asthmatic patients. 326 76

We have studied the role of prostaglandin E2 on the modulation of tumor necrosis factor by immunologically elicited and lipopolysaccharide treated murine macrophages. Indomethacin, a potent inhibitor of prostaglandin E2 production, caused a dose dependent augmentation of lipopolysaccharide induced tumor necrosis factor production (2-3 fold at 10(-7) molar). Tumor necrosis factor was released into the extracellular environment and no activity was found to be associated with membrane or cytosolic fractions. Prostaglandin E2 added to the lipopolysaccharide treated cultures suppressed tumor necrosis factor in a dose dependent manner. In these studies, 10(-7) molar PGE2 reduced tumor necrosis factor production to basal levels. These data suggest that PGE2 may be a potent autoregulatory factor that dramatically influences tumor necrosis factor production.
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PMID:Regulation of macrophage tumor necrosis factor production by prostaglandin E2. 345 61

Bradykinin (BK) and its fragment des-Arg9-BK failed to stimulate thymidine incorporation in all but one observed fibroblast cultures derived from human amniotic fluid or rabbit dermis. The rabbit dermis fibroblast line designated R51 acquired the capacity to increase its DNA synthesis in response to kinins after several weeks in culture. It was more sensitive to des-Arg9-BK than to BK and the effect of both peptides was antagonized by the analog Leu8, des-Arg9-BK; these features are shared with certain smooth muscle preparations responsive to kinins such as the rabbit aorta. Recently isolated rabbit dermis or human amniotic fibroblasts could not be made responsive to kinins by pre-incubating them with bacterial lipopolysaccharide. The line R51 released more PGE2 than baseline when stimulated with BK or des-Arg9-BK at low concentrations; it was also doubling faster than recently isolated cells of similar origin.
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PMID:Mitogenic effect of bradykinin and of des-Arg9-bradykinin on cultured fibroblasts. 346 53


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