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)

The mucosal immune system plays an important role in blocking the penetration of invasive organisms into various mucosal surfaces. Evidence now suggests neuroendocrine peptide hormones have immunomodulatory properties, including the ability to alter mucosal immunity. The potential for opioid compounds and corticotropic hormone (ACTH) to modulate mucosal immune function was investigated. We have found beta-endorphin, ACTH, and naltrindole (delta-class opioid receptor antagonist) to significantly suppress concanavalin A-stimulated Peyer's patch lymphocyte immunoglobulin production of IgA, IgG, and IgM isotypes. Oxymorphindole, a delta class opioid receptor agonist, significantly decreased IgM but not IgA or IgG production by the mitogen-stimulated Peyer's patch lymphocytes. Both oxymorphindole and naltrindole modestly reduced interleukin-2 receptor expression of concanavalin A- (Con A)-stimulated splenic and Peyer's patch lymphocytes. Neither compound appreciably affected immunoglobulin production by lipopolysaccharide-stimulated Peyer's patch lymphocytes. Collectively, these results indicate stress-related peptides such as ACTH and opioids may be involved in the regulation of immunoglobulin synthesis by Peyer's patch lymphocytes.
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PMID:Differential effect of opioids on immunoglobulin production by lymphocytes isolated from Peyer's patches and spleen. 217 75

The influence of dynorphin A (DYN) and related opioid peptides on the tumoricidal function of activated murine peritoneal exudate macrophages (PEM) was investigated. Addition of DYN to macrophage cultures previously activated with mixed alpha + beta-interferon (IFN-alpha/beta) and bacterial lipopolysaccharide (LPS) significantly enhanced their ability to lyse P815 murine mastocytoma cells in a 16 hr chromium-release assay. The effects of DYN were dependent on prior macrophage activation. Peptide subfragments of DYN were effective in a manner similar to that of the 17-amino-acid parent molecule, indicating that peptide interaction with either kappa or delta-opioid receptors on the effector cell is effective in potentiating lytic function. The involvement of opiate receptors was confirmed by inhibition of the effects of DYN and leucine enkephalin by the opioid receptor antagonist naloxone. Finally, in addition to IFN-alpha/beta-primed macrophages, DYN also augmented tumoricidal function in PEM primed for cytotoxicity by either gamma-interferon (IFN-gamma) or the calcium ionophore A23187, indicating that DYN potentiates function in activated macrophages independent of the specific mode of activation.
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PMID:Dynorphin and related opioid peptides enhance tumoricidal activity mediated by murine peritoneal macrophages. 243 27

The effect of a new, centrally acting analgesic, 2-n-pentyloxy-2-phenyl-4- methyl-morpholine (PM) on the humoral antibody isotype responses, mitogenic responses, and interleukin production and assay was studied. Treatment with this opioid agonist exerted a suppressive effect on the antibody responses to TD [sheep red blood cells (SRBC), fluoresceinated human gamma globulin (HGG-FITC)] and TI [fluoresceinated dextran (DEX-FITC), lipopolysaccharide (LPS)]antigens in mice. The suppression was found to be dose- and time-dependent for all antigens tested, suggesting that PM affected both T and B cells. PM impaired lymphocyte functions, as the in vitro T and B mitogen reactions were inhibited in a dose- and time-dependent manner in mice and rats. PM, even at the highest concentration used, could not completely inhibit the production of interleukin 1 (IL-1)-like activity, but it caused complete inhibition, in a dose-dependent manner, of the production of IL-2-like activity. In addition, PM inhibited the assays of both IL-1 and IL-2. Naloxone counteracted all immunosuppressive effects of PM in vivo and in vitro. From this it was concluded that PM operates on the immune system directly, via opioid receptor mechanisms. Our data suggest that immunosuppression by PM, an opioid agonist, may be exerted by an inhibition of interleukin action on lymphocytes, and they confirm the important role of opiate receptors in lymphocyte function.
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PMID:Immunosuppression by a novel analgesic-opioid agonist. 249 11

The effects of methionine-enkephalin (Met-Enk) on mitogenic and mixed lymphocyte culture (MLC) proliferation of splenocytes from Zn-deficient, restricted and control mice were evaluated. The data from this experiment show that Met-Enk can suppress the responses of splenocyte from the 3 groups to concanavalin A (Con A), but less inhibition was observed in the Zn-deficient group. Met-Enk can also enhance the responses to pokeweed mitogen (PWM) and decrease the response to lipopolysaccharide (LPS) in all groups. Alteration of proliferative responses to Con A and PWM were reversible in the presence of naloxone 10 mumol/L indicating that the effect of Met-Enk on cellular proliferation was mediated by the opioid receptor. In the proliferation of MLC, the response of lymphocytes from Zn-deficient mice was increased in the absence of Met-Enk and Met-Enk can suppress this increased response. It is therefore concluded that Met-Enk can modify the pattern of mitogenic responses and the alteration in Con A and MLC responses can be influenced by zinc deficiency.
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PMID:Methionine-enkephalin alteration of mitogenic and mixed lymphocyte culture responses in zinc-deficient mice. 253 55

The role of the neuropeptide beta-endorphin on interleukin 1 (IL-1) production by murine bone marrow-derived macrophages was assessed. Beta-endorphin by itself did not induce IL-1 generation. However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1. This enhancement by beta-endorphin was most evident when using suboptimal doses of LPS. Naloxone, a competitive inhibitor of beta-endorphin opioid receptor interactions, abrogated the enhancing effects of beta-endorphin on LPS-induced IL-1 production. Furthermore, LPS-induced IL-1 production by macrophages (in the absence of added beta-endorphin) was also partially inhibited following treatment with naloxone, suggesting that opioids derived from activated macrophages may also modulate IL-1 generation and secretion. Thus, beta-endorphin-opioid receptor interactions result in enhanced production of immunomodulators such as IL-1.
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PMID:Beta-endorphin regulates interleukin 1 production and release by murine bone marrow macrophages. 253 39

We investigated the effect of several opioid peptides on the activation of murine peritoneal exudate macrophages (M phi) in vitro. M phi were treated with interferon (IFN) as a priming agent and bacterial lipopolysaccharide (LPS) as a triggering agent in the presence or absence of opioid peptides. M phi activation was assessed by their tumoricidal activity. When treatment with IFN and LPS resulted in a high level activation of M phi, dynorphin-A exerted no further enhancing effect. When treatment induced only weak activation, however, dynorphin-A augmented the M phi activation. Leucine-enkephalin, methionine-enkephalin, and also beta-endorphin had augmenting effects. An opioid receptor antagonist, naloxone, reduced the effect of dynorphin-A and beta-endorphin. When M phi were treated sequentially with IFN and LPS, beta-endorphin operated in combination with LPS only. Moreover, beta-endorphin was effective for already activated M phi. These results indicate that opioid peptides act on M phi via classical opioid receptors, and that responsiveness to opioid peptides is induced in the triggering stage of M phi activation.
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PMID:Augmenting effect of opioid peptides on murine macrophage activation. 790 88

Previous studies have shown that morphine promotes the replication of human immunodeficiency virus (HIV)-1 in peripheral blood mononuclear cell cocultures. In the present study, we tested the hypothesis that morphine would amplify HIV-1 expression in the chronically infected promonocytic clone U1 when cocultured with lipopolysaccharide-stimulated human fetal brain cells. Marked upregulation of HIV-1 expression was observed in these cocultures (quantified by measurement of HIV-1 p24 antigen levels in supernatants), and treatment of brain cells with morphine resulted in a bell-shaped dose-dependent enhancement of viral expression. The mechanism of morphine's amplifying effect appears to be opioid receptor-mediated and to involve enhanced production of tumor necrosis factor-alpha by microglial cells.
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PMID:Morphine amplifies HIV-1 expression in chronically infected promonocytes cocultured with human brain cells. 812 Jan 38

The antinociceptive effect of lipopolysaccharide from Pantoea agglomerans (LPSp) in streptozotocin-induced diabetic mice was examined. Although subcutaneous (s.c.) administration of LPSp produced a dose-dependent inhibition of the tail-flick response in both non-diabetic and diabetic mice, the antinociceptive response was greater in diabetic mice than in non-diabetic mice. The antinociceptive effects of LPSp in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of naltrindole, a selective delta-opioid receptor antagonist or nor-binaltorphimine, a selective kappa-opioid receptor antagonist, but not by beta-funaltrexamine, a selective mu-opioid receptor antagonist. These results suggest that LPSp produces a marked antinociceptive effect in diabetic mice through the activation of delta- and kappa-opioid receptors.
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PMID:Antinociceptive effect of lipopolysaccharide from Pantoea agglomerans on streptozotocin-induced diabetic mice. 813 75

Opiates alter a variety of functional activities of the somatic immune system; within the central nervous system, however, their effects on immune responses are unknown. In the present study, we investigated the effect of morphine on the release of tumor necrosis factor (TNF)-alpha from murine neonatal microglia. Microglial cell cultures did not release TNF-alpha when incubated with morphine alone; however, an enhanced (P < .01) release of TNF-alpha was observed when cultures were first primed with morphine for 24 h and then stimulated with lipopolysaccharide. A bell-shaped dose-response curve was observed for the priming effect of morphine; maximal enhancement of TNF-alpha release (310 +/- 15% of control) was detected at a concentration of 10(-10) M morphine. Pretreatment of microglia for 30 min with opioid receptor antagonists (i.e. naloxone and beta-funaltrexamine) completely blocked the priming effect of morphine. In addition, morphine treatment amplified (P < .01) the priming effect of lipopolysaccharide on phorbol myristate acetate-triggered superoxide anion production by microglial cell cultures, and this effect was abrogated (P < .01) by anti-TNF-alpha antibody. Furthermore, culture supernatants derived from microglial cell cultures that had been treated with morphine before stimulation with lipopolysaccharide had an increased capacity to upregulate human immunodeficiency virus-1 expression in the latently infected promonocytic clone U1. This effect was also blocked by anti-TNF-alpha antibody. These findings suggest that morphine primes microglia for enhanced production of TNF-alpha which could alter several functional activities of these cells within the brain.
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PMID:Priming effect of morphine on the production of tumor necrosis factor-alpha by microglia: implications in respiratory burst activity and human immunodeficiency virus-1 expression. 816 25

Opiates modulate a variety of immune responses of peripheral blood mononuclear cells (PBMC). When PBMC were treated with morphine for 24 h, cells released less (P < 0.05) bioactive TNF, a cytokine important in host defense, in the following 24-h incubation period when stimulated with lipopolysaccharide and phytohemagglutinin. Morphine alone did not significantly alter the release of TNF from PBMC cultures. Pretreatment of PBMC cultures for 1 h with naloxone blocked (P < 0.05) the inhibitory effect of morphine on the release of TNF upon stimulation with phytohemagglutinin, but not with lipopolysaccharide, suggesting the involvement of an opioid receptor. The mechanism of morphine-induced suppression of TNF release appears to be counteracted by the effect of this opiate on the release of transforming growth factor (TGF)-beta, since antibodies to this immunoregulatory cytokine further enhanced morphine-related inhibition of TNF release. Taken together, these findings indicate that morphine suppresses the release of bioactive TNF from PBMC and that TGF-beta plays a modulatory role in this inhibitory process.
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PMID:Morphine inhibits the release of tumor necrosis factor in human peripheral blood mononuclear cell cultures. 838 31


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