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)

Secretion of unique eosinophil granule constituents may play a role in allergic and parasitic reactions. Therefore we have investigated possible mechanisms for regulation of secretion in eosinophils. A hemolytic plaque assay and an enzyme-linked immunospot (ELISPOT) assay were developed for detection of secreted eosinophil cationic protein (ECP) from single adherent eosinophils. The protein kinase C activator phorbol 12-myristate 13-acetate (PMA) induced release of ECP in a dose-dependent fashion but 4-alpha-PMA, an analogue that does not activate protein kinase C, did not cause degranulation. Staurosporine and K252a, inhibitors of protein kinase C, decreased PMA-induced ECP secretion. Low concentrations of cytochalasin B enhanced PMA-induced secretion but high concentrations had an inhibitory effect. The calcium ionophores A23187 and ionomycin were weaker secretagogues than PMA. Tumor necrosis factor, granulocyte-macrophage colony-stimulating factor, interleukin-3, interleukin-5, N-formylmethionyl-leucyl-phenylalanine, and lipopolysaccharide caused little or no degranulation in adherent eosinophils. Preincubation of eosinophils with antibodies to CD18, the common beta chain of leukocyte adhesion proteins, resulted in inhibition of PMA-induced ECP release from adherent cells. 1,2-Bis(O-aminophenyl)-ethane-ethane-N,N,N',N'-tetraacetic acid (BAPTA), an agent that acts intracellularly by chelation of calcium, also inhibited PMA-mediated ECP release. In conclusion, PMA induces release of ECP from single adherent eosinophils and the effect appears to be mediated via protein kinase C and, in contrast to that in neutrophils, to be dependent on CD11/CD18 leukocyte integrins.
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PMID:Phorbol ester-induced degranulation in adherent human eosinophil granulocytes is dependent on CD11/CD18 leukocyte integrins. 809 65

The effects of interleukin 1 alpha (IL-1 alpha), IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, and insulin growth factor-1 (IGF-1) on proliferation of mitogen-stimulated bovine peripheral blood mononuclear cells (PBMC) were determined. Four concentrations of each cytokine were incubated 48 or 96 h with PBMC alone or with PBMC and three concentrations of three different mitogens. The mitogens included concanavalin A (Con A) phytohemagglutinin (PHA), and Escherichia coli 055:B5 lipopolysaccharide (LPS). Proliferation of unstimulated PBMC was not affected by IL-1 alpha, IL-1 beta, IL-3, IL-5, IL-6, IL-8, and IGF-1 whereas IL-2, IL-4, and IL-7 increased proliferation. Incubation of PBMC with Con A plus IL-1 alpha, IL-2, IL-4, IL-7 or IL-8 increased proliferation when compared to PBMC that were incubated with either Con A or the cytokine alone. Interleukin-1 beta, IL-3, IL-5, IL-6 and IGF-1 did not influence proliferation of Con A-stimulated PBMC. Proliferation of PHA-stimulated PBMC was increased when PBMC were cultured with IL-2, IL-4 or IL-7, but not when cultured with IL-1 alpha, IL-1 beta, IL-3, IL-5, IL-6, IL-8 or IGF-1. Similar results occurred with LPS-stimulated PBMC in that proliferation induced by LPS was enhanced by IL-2 or IL-7, but not by any of the other cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of recombinant human cytokines on mitogen-induced bovine peripheral blood mononuclear cell proliferation. 814 6

The expression of alkaline phosphatase (APase) activity by purified B cells from lipopolysaccharide (LPS)-hyporesponsive C3H/HeJ mice was determined. Optimal APase activity was expressed after costimulation with interleukin-5 and dextran sulfate (DXS), whereas LPS, which is highly effective on B lymphocytes from normal mice, was unable to induce enzyme expression, even in the presence of DXS. The simultaneous determination by flow cytometry of both cellular APase, by using a fluorescent azo dye technique, and DNA content showed that APase was highly expressed by about one-tenth of cells in G1 phase, whereas it was present in more than 50% of cells in S and G2/M phases. The enzyme, as visualized by confocal microscopy after cell sorting on the basis of DNA content, was found to be localized mainly in vesicular structures distributed throughout the cytoplasm in G1 cells. It was distributed in patches and essentially localized at the cell periphery in S cells, whereas clear capping of activity was observed in G2/M cells.
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PMID:Expression and visualization during cell cycle progression of alkaline phosphatase in B lymphocytes from C3H/HeJ mice. 818 40

Prolonged consumption of ethanol (ETOH) results in alterations of host defense via immune modulation, increasing susceptibility to infection. In the present study, effects of chronic dietary ETOH on cytokine production by splenocytes and thymocytes, splenocyte and thymocyte proliferation induced by mitogens, splenic natural killer cell activity, and antibody production (IgA and IgG) were examined. C57BL/6 mice were fed 5% ETOH v/v in the Lieber-DeCarli liquid diet for 11 weeks. Release of interleukin (IL)-2, IL-5, IL-6, IL-10, and interferon (IFN)-gamma produced by concanavalin A (Con A) stimulated splenocytes was significantly decreased, whereas secretion of IL-4 was slightly decreased by chronic dietary ETOH compared with controls. Production of tumor necrosis factor-alpha and IL-6 by lipopolysaccharide-stimulated splenocytes was significantly and slightly decreased by ETOH compared with controls, respectively. Splenocyte and thymocyte proliferation induced by Con A was significantly inhibited by ETOH, whereas splenocyte proliferation induced by lipopolysaccharide was not affected. Natural killer cell activity was significantly inhibited by ETOH compared with controls. The production of IgA and IgG by splenocytes were also significantly decreased by ETOH compared with controls. The levels of IL-2, IL-4, and IL-6 produced by Con A-stimulated thymocytes were significantly reduced by dietary ETOH compared with control, whereas production of IFN-gamma by thymocytes was not affected. Our results suggest that chronic dietary ETOH alters the cytokine release, thereby impairing immune response and T-cell maturation, which increase host susceptibility to infection.
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PMID:Influence of chronic dietary ethanol on cytokine production by murine splenocytes and thymocytes. 819 29

Sea star factor (SSF), a protein of 39 kDa purified from macrophage-like coelomocytes of the echinoderm Asterias forbesi, has potent immunosuppressive effects on T-dependent but not T-independent antibody responses in vivo. SSF at a concentration of 0.5 microgram/ml markedly inhibits T-dependent antibody production in vitro by fluorescein (Flu)-specific B cells responding in clonal microculture to antigenic stimulation with Flu-conalbumin via the conalbumin-specific T cells D10.G4.1 (D10). At this concentration of SSF, Ig secretion induced by a T cell-independent stimulus, lipopolysaccharide (LPS), is not affected. Inhibition of antibody production in T-dependent microcultures by SSF can be completely overcome in a dose-dependent fashion by addition of lymphokine-rich supernatants from stimulated cultures of D10 cells. The possibility that SSF suppresses production of requisite cytokine growth factors from T cells was substantiated by the finding that SSF diminishes concentrations of stimulatory cytokines detectable in supernatants from antigen-stimulated cultures. Nevertheless, levels of intracytoplasmic mRNA for IL-4 and IL-5 are not detectably altered by concentrations of SSF that suppress antibody production. Furthermore, when cultures of D10 cells stimulated in the presence of SSF are subjected to freezing and thawing to release intracytoplasmic lymphokines, total levels of stimulatory cytokines are not lower than those in cultures without SSF. These results suggest that SSF inhibits antibody responses by limiting the availability of lymphokines produced by helper T cells. The mechanism for this inhibition may involve either direct effects of SSF on T cells or a block in effective T cell-B cell interaction.
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PMID:Sea star factor blocks development of T-dependent antibody secreting clones by preventing lymphokine secretion. 820 43

The mechanism whereby small resting (high buoyant density) murine B cells are induced to express interleukin-2 receptors (IL-2R) and to respond to IL-2 was addressed by staining with anti-IL-2R alpha and -IL-2R beta monoclonal antibodies (mAb), and using receptor-specific cDNA probes. Resting B cells expressed undetectable levels of both IL-2R alpha and beta chains on their surface and did not respond to IL-2, even at supra-physiological concentrations. Sepharose-coupled, but not streptavidin-cross-linked, plastic-adsorbed or soluble, anti-mu up-regulated the expression of IL-2R alpha and beta chains and mRNA to levels comparable to those seen in activated T cells. Anti-mu-stimulated B cells responded to IL-2 by incorporation of [3H]thymidine and high rate immunoglobulin (Ig) secretion. Both IL-5 (at optimal concentration) and suboptimal lipopolysaccharide (LPS; 20 ng/ml) induced surface expression of IL-2R alpha. The level of expression induced by IL-5 was equivalent to that on anti-Ig-activated B cells. Neither stimulus induced detectable expression of IL-2R beta, and neither induced B cells to respond to IL-2. IL-2R alpha expression was strongly enhanced, and low levels of IL-2R beta staining and mRNA were induced by the combination of LPS plus IL-5. LPS+IL-5-treated B cells responded to IL-2 by Ig secretion. This indicates that B cells regulate their responsiveness to IL-2 similarly to T cells, via the combined level of expression of IL-2R beta and IL-2R alpha. The synergy between IL-5 and LPS for B-cell responses shows a requirement for complementary stimuli such as would be provided by cytokines, and either cellular interaction or antigen recognition in regulation of B-cell responsiveness to IL-2.
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PMID:The acquisition of cytokine responsiveness by murine B cells: a role for antigen and IL-5 in the induction of IL-2 receptors. 820 11

Ethanol (ETOH) consumption has been associated with general suppression of the immune response, resulting in increased susceptibility to infection. Chronic dietary ETOH consumption may be one of the cofactors accelerating development of human acquired immune deficiency syndrome (AIDS) after retrovirus infection. Chronic dietary ETOH [5% (v/v)] in the Lieber-DeCarli liquid diet was fed female C57BL/6 mice inoculated with LP-BM5 retrovirus causing murine AIDS for 11 weeks. Because cytokines are key regulators of humoral and cellular immunity, their production by concanavalin A (ConA) and lipopolysaccharide (LPS)-induced splenocytes was measured by ELISA methods. Decreased levels of interleukin (IL)-2 caused by retrovirus infection remained unchanged. Elevated levels of IL-5 and IL-6 produced in vitro by ConA-stimulated spleen cells during retrovirus infection were significantly further increased by dietary ETOH. Elevated IL-4 due to retroviral infection were not affected by dietary ETOH. Increased production of IL-10 induced by retrovirus infection, however, was significantly reduced by dietary ETOH, whereas decreased release of interferon-tau induced by retrovirus infection was significantly enhanced. Elevated levels of tumor necrosis factor-alpha produced by LPS-stimulated splenocytes from retrovirus infected mice were significantly further increased by dietary ETOH, whereas levels of IL-6 by LPS-stimulated splenocytes were not affected. Suppressed T-cell proliferation caused by retrovirus infection was significantly reduced further by dietary ETOH. However, no effect of dietary ETOH was observed on decreased B-cell proliferation by retrovirus infection. These results suggest that dietary ETOH aggravates progression of immune dysfunction leading to AIDS, because dietary ETOH modifies production of immunological regulatory cytokines.
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PMID:Ethanol-induced modulation of cytokine production by splenocytes during murine retrovirus infection causing murine AIDS. 827 63

The capacity of exogenous interleukin-4 (IL-4) and IL-5 to augment the antigen-specific senescent Peyer's patch (PP), lamina propria (LP), and mesenteric lymph nodes (MLN) B cells was investigated in the present studies. CTx-primed lymphocytes in the PP, LP, and MLN were obtained from 4-and 24-month old C57BL/6J male mice, 14 days after oral immunization with cholera toxin (CTx). Cells were cultured optimally for 4 days either alone, with lipopolysaccharide (LPS), with LPS plus recombinant IL-4 or IL-5, or with LPS plus IL-4 or IL-5 plus monoclonal antibodies specific for the respective interleukin. Culture supernantants were tested for IgA and IgG anti-CTx antibodies by an ELISA assay. The data indicated impaired antibody responses of aged PP and MLN B cells by the lack of LPS plus IL-4 induced enhancement of anti-CTx IgG antibody production as compared with the young group. For anti-CTx IgA production, aged LP and MLN B cells did not respond equally as well to LPS plus IL-5 stimulation as the young group. In contrast, aged PP B cells responded equally as well by anti-CTx IgA production to LPS plus IL-5 stimulation as the young group. Both anti-IL-4 and anti-IL-5 Mabs blocked the respective IL-4 and IL-5-induced enhancement of antigen-specific IgG or IgA antibody production. The findings suggest a regional dichotomy of IL-5 induced enhancement of aged IgA-producing B cells specific for CTx in the Peyer's patches, mesenteric lymph nodes, and lamina propria.
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PMID:Regional dichotomy of interleukin-4 and -5 regulation of senescent B cell responses specific for cholera toxin in Peyer's patches, lamina propria, and mesenteric lymph nodes. 834 71

The effects of the immunosuppressant mycophenolate mofetil (MPAM, RS-61443) on cytokine production at the single cell level were assessed using in vitro activated human mononuclear cells. Cytokine production was studied with UV microscopy of fixed and permeabilized cells stained with cytokine specific monoclonal antibodies (mAbs). The cytokines evaluated included interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10 interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), TNF-beta, and granulocyte macrophage-colony stimulating factor (GM-CSF). MPAM exhibited a marked antiproliferative effect without cytotoxicity in all mononuclear cell cultures. Six to 24 hours after stimulation with the superantigen Staphylococcus aureus enterotoxin A (SEA), most cytokine production was unaffected by MPAM at therapeutic concentrations (10(-6) M), with the exception of GM-CSF. In contrast, by 48 h after antigen activation, MPAM significantly inhibited all studied cytokine production (p < 0.05). Cyclosporin A (CsA), used as a control at a concentration of 100 ng/ml, inhibited production of all studied cytokines, at all time points. Monokine production after lipopolysaccharide (LPS) stimulation was unaffected by MPAM. Similarly, the production of most of the cytokines studied after mitogen stimulation with phorbol ester (PMA) plus calcium ionophore (ionomycin) was not affected by MPAM, in comparison to CsA which demonstrated significant inhibition of all cytokines tested under these conditions. However, a late inhibitory effect on IL-3 production was seen by MPAM at 48 h after mitogenic stimulation. Further observations are required to explain the divergent results on cytokine production by MPAM in superantigen-activated and mitogen-activated human mononuclear cells.
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PMID:Effect of mycophenolate mofetil (RS-61443) on cytokine production: inhibition of superantigen-induced cytokines. 840 81

Extracts prepared from the salivary glands (SGE) of partially fed adult female Rhipicephalus appendiculatus ticks reduced the expression by human peripheral blood leukocytes 9PBLs) of lipopolysaccharide (LPS)-stimulated cytokine mRNA. Treatment with SGE had no obvious effect on cytokine mRNA production when compared with untreated PBLs. LPS treatment induced or increased mRNA production for IFN alpha, TNF-alpha, IL-1 alpha, IL-1 beta, IL-5, IL-6, IL-7 and IL-8. All the LPS-stimulated cytokine mRNAs were reduced when treated with a mixture of LPS and SGE. The results indicate the potential of ticks in modulating the cytokine network of their vertebrate hosts, possibly to facilitate blood feeding.
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PMID:Ixodid tick salivary gland extracts inhibit production of lipopolysaccharide-induced mRNA of several different human cytokines. 855 60


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