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)

Antisera against isolated outer membrane (OM) proteins I and II of Escherichia coli O26 K60 were elicited in rabbits. Antisera obtained after intramuscular administration with Freund's complete adjuvant showed high titres of specific antibodies. Intravenous administration of the same preparations yielded a considerable antibody response against bacterial lipopolysaccharide, a minor contaminant of the protein preparations. Antibody titres against OM proteins I and II, lipopolysaccharide and murein-lipoprotein were determined by the enzyme-linked immunosorbent assay (ELISA) in these sera, and in antisera elicited against whole formaldehyde-fixed bacteria or isolated OM. Comparison of ELISA with single radial immunodiffusion and interfacial immunoprecipitation tests revealed that ELISA was not only the most uniformly applicable, but also the most specific and the most convenient method. In double diffusion tests no cross-reactivity between proteins I and II was seen. Antibodies against proteins I and II, lipopolysaccharide and lipoprotein could be specifically absorbed from the sera with the appropriate antigen preparations. Absorption experiments with intact E. coli O26 K60, Tris/EDTA-sheared bacteria and isolated OM revealed that antibodies against protein I were hardly absorbed at all probably because the antibody, evoked against denatured protein I, did not react with the protein in its native configuration. Antibodies against protein II and lipoprotein were absorbed by intact as well as by sheared bacteria, but to a much greater extent by isolated OM, which indicates that these OM components are accessible from the outside, but that they are situated relatively deep in the OM structure.
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PMID:Preparation and quantitative determination of antibodies against major outer mambranes proteins of Escherichia coli O26 K60. 677 43

Previous findings provided evidence that bacterial lipopolysaccharide (LPS)-activated human monocytes are able to upregulate autologous polymorphonuclear (PMN) phagocytic ability via cell-to-cell contact mechanisms mediated by membrane (m)-associated cytokines (CKs), such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-1 beta, IL-6 and IL-8. Consequently, the role of the lymphocyte function-associated antigen (LFA)-1 molecule on the monocyte (Mo)-PMN interplay was evaluated. In the first step, lipid A (LA)-stimulated Mo were pretreated with anti-recombinant human (Rhu) LFA-1 alpha monoclonal antibody (MoAb), and the enhanced phagocytic activity of PMN was abrogated. Pretreatment of unstimulated Mo with the same MoAb led to a reduction of PMN phagocytosis. In the second step, the role of m-LFA-1 on PMN was investigated with regard to Mo modulation. Anti-Rhu LFA-1 alpha MoAb was supplemented to LA-activated and unstimulated PMN, respectively, before coculturing with autologous LA-activated Mo. The addition of anti-Rhu LFA-1 alpha MoAb gave rise to a significant decrease in PMN phagocytosis regardless of PMN activation. These data suggest that, besides m-CKs, LFA-1 present on Mo and PMN might be involved in the mutual interplay between PMN and Mo.
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PMID:Role of lymphocyte function-associated antigen-1 on the interplay between lipid A-activated monocytes and polymorphonuclear cells. 747 67

Interleukin-8 is a neutrophil chemoattractant that has been implicated in the pathogenesis of alcoholic hepatitis. The mechanism of ethanol-induced interleukin-8 production in liver is uncertain, although hepatocytes and Kupffer cells have both been proposed as sources of the chemokine. In this study we investigated whether short-term ethanol exposure stimulates production of rat interleukin-8 [cytokine-induced neutrophil chemoattractant (CINC)] by normal rat hepatocytes and Kupffer cells in primary culture. Initial experiments verified that hepatocytes and Kupffer cells produce CINC in response to cytokines or lipopolysaccharide. Ethanol, by contrast, failed to stimulate CINC secretion by either cell type even at concentrations as high as 100 mM. Although ethanol had no direct effect on liver cell CINC production, conditioned medium from ethanol-treated hepatocytes induced a threefold rise in CINC production by Kupffer cells. The increase was abrogated when hepatocytes were treated with ethanol and the metabolic inhibitor 4-methylpyrazole. The results suggest that the mechanism of ethanol-induced CINC production is indirect, involving ethanol oxidation and communication between hepatocytes and Kupffer cells.
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PMID:Rat hepatocytes and Kupffer cells interact to produce interleukin-8 (CINC) in the setting of ethanol. 748 3

Interleukin (IL)-3 stimulates hemopoiesis in vitro. However, IL-3 is not normally found in bone marrow, raising doubts as to the in vivo role of IL-3. We have found that human umbilical vein endothelial cells (HUVEC) express functional high-affinity receptors for IL-3 after stimulation with tumor necrosis factor alpha (TNF-alpha), IL-1 beta, or lipopolysaccharide, and that this receptor is involved in inflammatory phenomena. TNF-alpha caused time- and dose-dependent up-regulation of mRNA for the IL-3 receptor alpha and beta chains, with maximal effects occurring 16-36 h after stimulation with TNF-alpha at 100 units/ml. Induction of mRNA correlated with protein expression on the cell surface as judged by monoclonal antibody staining and by the ability of HUVEC to specifically bind 125I-labeled IL-3. Scatchard analysis under optimal conditions of TNF-alpha stimulation revealed approximately 1500 IL-3 receptors per cell, which were of a high-affinity class (Kd = 500 pM) only. In contrast to a previous report, receptors for granulocyte-macrophage colony-stimulating factor could not be detected. IL-3 binding to TNF-alpha-activated HUVEC enhanced IL-8 production, E-selection expression, and neutrophil transmigration. The selective induction of a functional IL-3 receptor on endothelial cells suggests that, beyond hemopoiesis, IL-3 may have an important role in chronic inflammation and in allergic diseases.
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PMID:The receptor for interleukin 3 is selectively induced in human endothelial cells by tumor necrosis factor alpha and potentiates interleukin 8 secretion and neutrophil transmigration. 824 92

Interleukin-8 (IL-8) is an important mediator of inflammation and has been shown to be a potent chemotactic/cell activator for polymorphonuclear neutrophils (PMNs). T lymphocytes, and basophils. Cellular sources of IL-8 include monocytes, PMNs, endothelial cells, epithelial cells, and keratinocytes when stimulated by factors such as lipopolysaccharide, IL-1, and tumor necrosis factor-alpha. This report demonstrates that C5a, in addition to being a direct mediator of inflammation, can induce both IL-8 synthesis and high levels of release from monocytes. Natural human C5a and a synthetic C-terminal analogue peptide of C5a each induced IL-8 synthesis and release from CD14+ human peripheral blood mononuclear cells. Antigenic reactivity based on enzyme-linked immunosorbent assay gave evidence that IL-8 was present in the culture supernatants of stimulated peripheral blood mononuclear cells. Proof that supernatant levels of IL-8 attain biologically significant quantities was provided by human PMN chemotaxis assays. The quantity of IL-8 recovered from C5a-activated monocytes in peripheral blood mononuclear cells is up to 1,000-fold greater than that released from comparable numbers of PMNs under similar conditions. Therefore, IL-8 released from C5a-activated monocytes may play a significant role in expanding and prolonging cellular infiltration and activation at sites of infection, inflammation, or tissue injury. This observation suggests an important humoral amplification loop for inflammatory events involving both complement activation and cytokine release.
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PMID:Induction of interleukin-8 synthesis from monocytes by human C5a anaphylatoxin. 750 86

Human monocytes (M phi) require stimulation with substances such as bacterial endotoxin [LPS (lipopolysaccharide)] to produce angiogenic activity. In this study, we report that stimulation of M phi with LPS (5 micrograms/ml) in the absence of L-arginine greatly reduced their production of angiogenic activity, as assessed in vivo in rat corneas and in vitro by chemotaxis of human umbilical vein endothelial cells (HU-VECs). D-Arginine did not substitute for L-arginine in the production of angiogenic activity. The nitric oxide synthase (NO synthase, EC 1.14-13.39) inhibitors NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine methyl ester (L-NAME) both inhibited the production of angiogenic activity by LPS-stimulated M phi in the presence of L-arginine, suggesting the involvement of this enzyme in the pathway that generates angiogenic activity. Neither of these substances directly inhibited the M phi-derived angiogenic activity. LPS-induced production of the cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 8 (IL-8) was not significantly reduced when M phi were incubated in the absence of L-arginine. Similarly, L-NMMA and L-NAME did not significantly reduce the LPS-induced production of these cytokines by M phi in the presence of L-arginine. These results suggest that the LPS-stimulation-dependent generation of angiogenic activity by M phi requires an L-arginine-dependent NO-synthase effector mechanism that may be independent of the generation of TNF-alpha and IL-8.
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PMID:Production of angiogenic activity by human monocytes requires an L-arginine/nitric oxide-synthase-dependent effector mechanism. 751 98

Chronic idiopathic neutropenia is an uncommon condition characterized by a low level of neutrophils without any causative disease. We report the details of 4 patients whose stromal cytokine mRNA expressions were examined by reverse transcription polymerase chain reaction. Three patients showed a lower expression of granulocyte colony-stimulating factor (G-CSF) mRNA both in constructive and lipopolysaccharide (LPS)-induced conditions and normal colony forming unit-granulocyte-macrophage (CFU-GM) from the bone marrow cells. One patient showed an increase of G-CSF mRNA and a decrease of CFU-GM. No abnormal expression of other cytokines including interleukin (IL)-1 beta, IL-6 and IL-8 were observed. These findings indicate that cytokine mRNA analysis of stromal cells is useful for elucidation of the etiology.
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PMID:Chronic idiopathic neutropenia associated with abnormal expression of granulocyte colony-stimulating factor mRNA of bone marrow stromal cells. 751 24

The mechanisms by which dietary fatty acids can modulate atherogenesis and inflammation are poorly understood. Induction in endothelial cells of adhesion molecules for circulating leukocytes and of inflammatory mediators by cytokines probably contributes to the early phases of atherogenesis and inflammation. We report here that incorporation into cellular lipids of docosahexaenoic acid (DHA), a specific fatty acid of the omega 3 family, decreases cytokine-induced expression of endothelial leukocyte adhesion molecules, secretion of inflammatory mediators, and leukocyte adhesion to cultured endothelial cells. DHA, but not eicosapentaenoic acid, decreased in a dose- and time-dependent fashion the expression of vascular cell adhesion molecule 1 (VCAM-1) induced by interleukin (IL)-1, tumor necrosis factor (TNF), IL-4, or bacterial lipopolysaccharide, with half-maximum inhibition at < 10 mumol/L. This reduction required prolonged (24- to 96-hour) exposure of endothelial cells to DHA and correlated with the degree of DHA incorporation into cellular lipids. DHA also limited cytokine-stimulated endothelial cell expression of E-selectin and intercellular adhesion molecule 1 and the secretion of IL-6 and IL-8 into the medium but not the surface expression of constitutive surface molecules. Cyclooxygenase inhibition did not block the effect of DHA on VCAM-1. In parallel with reduced surface VCAM-1 protein expression, DHA reduced VCAM-1 mRNA induction by IL-1 or TNF. DHA treatment also reduced the adhesion of human monocytes and of monocytic U937 cells to cytokine-stimulated endothelial cells. These properties of DHA may contribute to antiatherogenic and anti-inflammatory effects of omega 3 fatty acids.
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PMID:The omega-3 fatty acid docosahexaenoate reduces cytokine-induced expression of proatherogenic and proinflammatory proteins in human endothelial cells. 752 49

We have examined basal and lipopolysaccharide (LPS)-induced release of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), interleukin 8 (IL-8), tumour necrosis factor-alpha (TNF-alpha) and soluble CD14 (sCD14) in whole blood and peripheral blood mononuclear cells (PBMC) from 20 persons with either high (1.62-2.47 mmol/L) or low (0.43-1.29 mmol/L) levels of high-density lipoprotein (HDL). Whole blood was incubated at 37 degrees C for 2 h with 100 ng LPS/ml, while PBMC were incubated with 100 ng LPS/ml for up to 160 h. The LPS-induced release of IL-1 beta, IL-6, IL-8 and TNF-alpha into plasma showed no differences between the two HDL-groups; whereas levels of sCD14 were significantly higher in plasma in persons with low HDL (P < 0.01). PBMC incubated with LPS showed a significantly higher release of IL-1 beta (P = 0.01) and IL-6 (P = 0.02) in persons with high HDL at all sampling times. sCD14 was found not to be released by PBMC. These findings indicate that PBMC from persons with high or low levels of HDL have different functional properties, possibly of importance in inflammation and atherogenesis.
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PMID:LPS-induced release of IL-1 beta, IL-6, IL-8, TNF-alpha and sCD14 in whole blood and PBMC from persons with high or low levels of HDL-lipoprotein. 753 60

This study examined effects of blood-contacting materials on the monocyte reaction following the first contact of human blood with hollow fibre dialyser membranes under pyrogen-free conditions. Membrane materials were the unchanged regenerated cellulose, the synthetic polysulphone (PS), a positively charged diethylaminoethyl cellulose (DEAE-C), the negatively charged carboxymethyl cellulose (CMC) and acrylonitrile copolymer (AN). The experimental system involved perfusion with human fresh venous blood through different modules containing the materials in the form of hollow fibre membranes. Extracellular and intracellular aspects of blood reactions after the first contact with the materials were investigated in Ficoll-separated granulocytes and peripheral blood mononuclear cells. Investigations were done by release reactions of platelet activating factor (PAF), oxygen radical (O2-), leukotriene B4, prostaglandin E2 (PGE2) and cytokines (IL-1 beta, TNF-alpha, IL-6). The intracellular activation of peripheral blood mononuclear cells was done by mRNA transcription of IL-1 beta, TNF-alpha, IL-6, IL-8 and beta 2-microglobulin (beta 2-MG). From the set of parameters, release reactions were only measurable for PAF, PGE2 and O2- if a second stimulus (phorbol myristate acetate, lipopolysaccharide, zymosan and calcium ionophore) was used after blood-membrane interaction. Although the extent of the release reaction was weak, negatively charged membranes were, in general, more active. All dialysers exhibited the same increase in beta 2-MG mRNA transcription, suggesting that all blood-contacting membranes initiate the gene expression of beta 2-MG at the same level. TNF-alpha, IL-6, IL-1 beta and IL-8 mRNAs were demonstrated in the AN and CMC membranes rather than the other materials, which exhibit a lower transcription than the tubing set. As has been found, an enhanced generation of PGE2 for both CMC and AN membranes supports, therefore, the concept of an effect of the negative charges of the materials in the gene expression of cytokines. However, this initiation does not lead to the generation of cytokines, even after stimulation with pyrogens.
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PMID:Effect of dialyser membranes on extracellular and intracellular granulocyte and monocyte activation in ex vivo pyrogen-free conditions. 753 Sep 99


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