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)

Our study indicated that the newly synthesized E-receptor, as measured with 125I-labeled monoclonal anti-E receptor antibody, on activated T lymphocytes were responsible for forming stable E-rosettes at 37 degrees C. Maximum induction of new E-receptor expression required at least 50 hr of culture with polyclonal T-cell activators, phytohemagglutinin, or phorbol myristate acetate. Polyclonal B-cell activator, lipopolysaccharide were not able to induce new E-receptor expression on the surface of T lymphocytes. The expression of the new E-receptor paralleled with the induction of Tac antigen expression. Interleukins 1 and 2 or Interferon-gamma were not able to initiate the induction of new E-receptors. However, a neuropeptide, endorphin exhibited biphasic effect on modulating the E-receptor expression, in the absence of polyclonal activators. As is the case with Tac antigen expression, induction of new E-receptor antigen may be a marker for activated T lymphocytes.
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PMID:Modulation of E-receptor expression on activated T lymphocytes. 300 Jun 64

Interferon-gamma (IFN-gamma) is a macrophage-activating factor that has also been shown to act on endothelial cells (EC). Interleukin 1 (IL 1), first described as a monocyte product, is also produced by EC after stimulation by lipopolysaccharide (LPS). In this study, the effect of IFN-gamma on the release of IL 1 by EC stimulated with LPS has been investigated. Although IFN-gamma did not stimulate the release of IL 1 or increase the apparent intracellular pool of IL 1 when incubated with EC, there was an increase in the amount of IL 1 released when cells preincubated with IFN-gamma were stimulated with LPS. The effect of IFN-gamma increased with concentration (1 to 1000 U/ml) and with duration of preincubation (24 to 96 hr). The presence of IFN-gamma was not required during the stimulation with LPS. When EC were cultured without IFN-gamma for increasing time periods up to 96 hr, the amount of IL 1 released by EC on subsequent stimulation with LPS progressively decreased. Addition of as little as 1 U/ml of IFN-gamma, however, prevented the loss in capacity of EC to secrete IL 1 when stimulated with LPS. In vivo, EC are involved in the emigration of mononuclear cells from the blood to inflammatory sites. Because IL 1 is chemotactic for lymphocytes and also increases the binding of lymphocytes to EC, activation of EC by T cell-derived factors such as IFN-gamma may augment lymphocyte emigration by increasing the release of IL 1 at the blood-tissue interface.
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PMID:Immune interferon enhances the production of interleukin 1 by human endothelial cells stimulated with lipopolysaccharide. 309 84

The expression of early "competence" genes has been examined in murine peritoneal macrophages treated with bacterial lipopolysaccharide (LPS). This set of genes (e.g., c-myc, c-fos, r-fos, JE, and KC) were first described in BALB/c 3T3 cells treated with platelet-derived growth factor. We have previously reported that LPS induces the rapid and transient expression of both c-myc and c-fos in macrophages. In the present report, we present evidence demonstrating that the mRNA for JE and KC are also induced in macrophages after treatment of LPS. The r-fos gene was not detectably induced by LPS under the experimental conditions used in this study. The induction of JE and KC were dependent upon the dose of LPS and exhibited different time courses. mRNA for both KC and JE was induced within 30 min from the initiation of treatment. Although mRNA for JE continued to accumulate for up to 24 hr, mRNA for KC was optimally seen after 60 min and had disappeared by 4 hr. c-fos, JE, and KC mRNA were all inducible by a variety of structurally diverse but functionally similar agents (e.g., heat killed Listeria monocytogenes, maleyl-bovine serum albumin, and fucoidan). Interferon-gamma, a potent but functionally distinct stimulus of macrophage activation, did not effect the expression of JE or KC mRNA. The expression of mRNA for c-fos could be readily induced by treatment of macrophages with phorbol myristate acetate (PMA) alone and that for JE by PMA plus the inophore A23187; mRNA for KC was largely unaffected by these agents. These results suggest that expression of the c-fos and JE genes are regulated by products of polyphosphoinositide hydrolysis. The difference between c-fos or JE and KC raises the possibility that LPS may stimulate at least two independent routes of early gene expression. LPS does not promote macrophage proliferative activity alone, and in fact inhibits the proliferative response to the macrophage growth factor colony-stimulating factor 1. Taken together these findings suggest that the products of these genes may function in the acquisition of competence for highly differentiated functions in addition to that for cell division.
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PMID:The effect of LPS on expression of the early "competence" genes JE and KC in murine peritoneal macrophages. 310 79

Interferon-gamma (IFN-gamma) can act to potentiate lipopolysaccharide (LPS)-stimulated processes in mononuclear phagocytes, including interleukin-1 release and tumoricidal activity. The present investigation examined the capacity of IFN-gamma to modulate LPS-stimulated prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) release from counterflow isolated human monocytes. The release of PGE2 and TxB2 was compared for cells incubated with IFN-gamma prior to treatment with LPS and for cells treated simultaneously with IFN-gamma and LPS. Treatment of cells with IFN-gamma prior to stimulation with LPS (10 micrograms/ml, Salmonella typhimurium) resulted in elevated prostaglandin E (by immunoassay) and [3H]PGE2 release from monocytes when compared with LPS-treated cultures. In contrast, IFN-gamma pretreatment did not potentiate labeled or immunoreactive TxB2 release from LPS-treated monocytes. IFN-gamma pretreatment without LPS stimulation did not result in elevated eicosanoid release over controls. In addition, continuous treatment of monocytes with both IFN-gamma and LPS did not result in greater release of PGE2 and TxB2 than the summed individual effects of IFN-gamma and LPS. These results indicate that IFN-gamma selectively potentiates LPS-stimulated arachidonic acid conversion to PGE2 and not TxB2 in human monocytes. This effect was observed only for monocytes pretreated with IFN-gamma prior to stimulation with LPS.
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PMID:Interferon-gamma potentiation of lipopolysaccharide-induced eicosanoid release from human monocytes. 310 16

Human endothelial cells and dermal fibroblasts both expressed a membrane-associated interleukin 1 (IL-1) activity when stimulated with either recombinant tumor necrosis factor (TNF) or recombinant lymphotoxin but stimulated endothelial cells expressed significantly more membrane IL-1 per cell than did fibroblasts. Lipopolysaccharide induced membrane IL-1 activity on endothelial cells but not fibroblasts. Interferon-gamma treatment of endothelial cells and fibroblasts had no direct effect on membrane IL-1 expression and little effect when used as a pretreatment for TNF or lipopolysaccharide stimulation. Endothelial cell membrane IL-1 activity was induced within 24 hr of culture with TNF or lipopolysaccharide, and increased up to 72 hr of incubation. Antibodies raised against human monocyte-derived IL-1 species neutralized the membrane IL-1 activity of TNF-stimulated endothelial cells. Both absorption studies and neutralization with specific sera indicated that endothelial cell membrane IL-1 is structurally related to IL-1 alpha. Endothelial cells expressed both IL-1 beta mRNA in response to TNF, lymphotoxin, and recombinant IL-1 species, as detected by Northern blot analysis. These studies demonstrate that endothelial cells can be activated to express a cell-surface IL-1 activity which is structurally, as well as functionally, related to the secreted form of IL-1.
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PMID:Membrane interleukin 1 induction on human endothelial cells and dermal fibroblasts. 311 78

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

Macrophages are pivotal cells in interactions of man and leishmania. Leishmanial disease results from intracellular infection of macrophages: parasitized cells are seen in smears or biopsy specimens of lesions; macrophages cultured in vitro support replication of parasites. Paradoxically, parasite destruction is also mediated by macrophages, which become highly cytotoxic after exposure to immune lymphocytes or their lymphokine (LK) products. The precise molecular mechanisms by which lymphocytes or LK induce macrophage activation for leishmanicidal activity, however, are not yet known. We analyzed interactions of leishmania amastigotes with human monocytes cultured in vitro as a nonadherent cell pellet. Leishmania donovani and L. major replicated in freshly isolated monocytes. Monocytes treated with greater than 200 IU/ml of the LK, human Interferon-gamma (IFN-gamma), destroyed tumor cells and L. donovani, but not L. major. Phorbol myristate acetate, endotoxic bacterial lipopolysaccharide, and recombinant human IFN-alpha and IFN-beta did not induce cytotoxicity. The time course for induction of cytotoxicity contrasted sharply with that of previously described monocyte antileishmanial activity: IFN-gamma induced cytotoxicity even when added after infection with L. donovani; induction of cytotoxicity did not require that IFN-gamma be present throughout the period of culture after infection: a 30-min preinfection pulse of IFN-gamma was sufficient to induce 70% of maximal activity; and freshly isolated monocytes and cells cultured for up to 4 days in vitro prior to infection and IFN-gamma treatment were equally responsive to IFN-gamma. These studies provide convincing evidence for intracellular cytotoxicity for L. donovani by freshly isolated human monocytes. This system provides an important base for further analysis of induction and expression of cytotoxic mechanisms against leishmania and other intracellular organisms that cause human disease.
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PMID:Human monocyte activation for cytotoxicity against intracellular Leishmania donovani amastigotes: induction of microbicidal activity by interferon-gamma. 392 73

Interferon-gamma (IFN-gamma) is a cytokine known to exert an important immunological role on astrocytes and oligodendrocytes. As a receptor for IFN-gamma has been demonstrated on murine astrocytes, we have searched for a specific receptor on the cell surface of pure mouse oligodendrocytes maintained in tissue culture. Using recombinant murine IFN-gamma labelled with 125I, we have established the basic physicochemical parameters of the binding. A single receptor was found with a Kd of 1 x 10(-9) M. The number of receptors per cell was 3000-4000 and its molecular weight, as determined by cross-linking experiments, is 87,000. The binding of IFN-gamma to its oligodendrocyte receptor is saturable, specific and temperature-dependent. The receptor-IFN-gamma complex is quickly endocytosed at 37 degrees (the half-time of maximal internalization is around 1 min). Some cytokines, such as interleukin-1 alpha and interleukin-6, up-regulated the expression of the oligodendrocyte receptor, but others, such as tumour necrosis factor-alpha, did not. A dramatic increase in receptor expression is induced by lipopolysaccharide but it is not detectable after treatment with concanavalin A.
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PMID:Expression of interferon-gamma receptors on murine oligodendrocytes and its regulation by cytokines and mitogens. 749 Jan 26

We have examined the effects of the herbal medicine sho-saiko-to (SST) on nitric oxide (NO) biosynthesis in rat hepatocytes by measuring the stable end-product nitrite and the mRNA of inducible NO synthase (iNOS). Interferon-gamma (IFN) by itself failed to induce NO synthesis (IFN: 1-1,000 u/ml). SST also did not elicit NO synthesis at concentrations up to 300 micrograms/ml when administered alone, but dose-dependently induced NO production in the presence of IFN. Whereas SST or IFN induced barely detectable levels of iNOS mRNA when administered alone, a combination of SST and IFN markedly induced iNOS mRNA in the cells. SST also modestly increased NO synthesis caused by interleukin-1 or bacterial lipopolysaccharide as a single agent, or in combination with IFN. On the other hand, SST had no effects on the NO synthesis produced by iNOS which were already induced. Thus, we found that SST stimulates cultured hepatocytes to produce NO by inducing iNOS gene expression under appropriate conditions. The capability of SST to induce NO biosynthesis might be related to the therapeutic efficacy of SST on the liver diseases.
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PMID:The herbal medicine sho-saiko-to induces nitric oxide synthase in rat hepatocytes. 753 74

Nitric oxide (.NO) is a short-lived mediator that can be induced by different cytokines and lipopolysaccharide (LPS) in a variety of cell types and produces many physiological and metabolic changes in target cells. In the current study, we show that a combination of cytokines, LPS, and zymosan-activated serum (ZAS; called for convenience cytomix Z) induces production of high concentrations of the NO oxidation products nitrite (NO2-) and nitrate (NO3-) by cultured rat fetal lung epithelial type II cells in a time-dependent fashion. Interferon-gamma and tumor necrosis factor-alpha alone did not significantly affect .NO synthesis, whereas ZAS, LPS, and interleukin-1 beta caused only a modest increase in formation of .NO oxidation products. Production of NO2- and NO3- was inhibited by NG-monomethyl-L-arginine and cyclohexmide. After exposure of these cells to a combination of the above cytokines, Escherichia coli LPS, and ZAS (cytomix Z), enhanced inducible nitric oxide synthase (iNOS) expression was indicated by an elevation in steady-state mRNA specific for iNOS (via Northern blot analysis) and increased immunofluorescence for iNOS after cell permeabilization, incubation with anti-iNOS antibody, and treatment with Cy3.18-conjugated rabbit-specific antibody. The extent of inflammatory mediator-induced.NO production by alveolar epithelium, which exceeds that of other lung cell types, reveals new insight into mechanisms of pulmonary host defense and pathways of free radical-mediated lung injury.
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PMID:Pulmonary alveolar epithelial inducible NO synthase gene expression: regulation by inflammatory mediators. 753 97


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