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)

Friend leukemia virus (FLV) leukemogenesis was prevented by treatment of the virus with Concanavalin A (Con A). Mice infected with the lectin-treated virus, however, showed evidence of a dormant infection since infectious virus could be recovered for as long as 100 days. Humoral immune responses to sheep erythrocytes (SRBC), a thymus-dependent antigen, and to E. coli lipopolysaccharide (LPS), a thymus-independent antigen, were depressed (approximately 80-90%) in mice given the Con A-treated FLV. Cell transfer studies indicated that the impaired responsiveness to SRBC was related to a defect in B-lymphocyte function, similar to the impairment in mice infected with untreated FLV. The mitogenic response of splenocytes from Con A-FLV mice to E. coli LPS was also depressed as was the ability of Ig-bearing spleen cells to redistribute these immunoglobulin receptors into polar caps. The impaired immune responsiveness in the Con A-FLV infected mice appeared associated with the persistent virus infection and not to neoplastic transformation generally associated with leukemogenic process.
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PMID:Discussion paper: impairment of B-lymphocyte functions in concanavalin A-treated friend virus infected mice. 108 87

The primary antibody response of BALB/c splenocytes to sheep erythrocytes in vitro was suppressed by infection with Friend leukemia virus (FLV), with the response capacity decreasing with increasing duration of infection. The acquisition of normal antibody responses was amplified by macrophage-produced antibody response helper factor(s). FLV-infected mice were treated with bacterial lipopolysaccharide to induce the release of these helper factors into the serum. Similar to the loss of antibody response capacity by their splenocytes, the FLV-infected mice progressively lost the ability to produce helper factors in response to lipopolysaccharide. In vitro cultures of FLV-infected cells also showed a depressed ability to produce helper factor activity both spontaneously and in response to lipopolysaccharide stimulation. The reconstitution of normal levels of exogenous helper factors to FLV-infected splenocytes restored the antibody response to normal or even elevated levels. These studies indicate that the mechanism for suppression of antibody responses by FLV involves the depression of antibody response helper factor production.
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PMID:Role of antibody response helper factors in immunosuppressive effects of friend leukemia virus. 622 Sep 70

Goat and rat antisera directed against Friend leukemia virus (anti-FLV) were found to be B-lymphocyte mitogens stimulating DNA synthesis in these cells but not in T lymphocytes. Membrane fluorescence microscopy showed that anti-FLV reacts with a subset of B lymphocytes of which the majority express immunoglobulin mu chains. The mitogenic effect was found with all mouse strains tested including 129 and AKR. Absorption experiments with purified viruses indicated that the mitogenic effect is specific for an antigen present in murine leukemia viruses of the FMR subgroup. In absorption experiments with viable cells, the antigen involved in mitogenicity was found to be expressed on Friend erythroleukemia cell lines (4/4) and on myelomas (2/2) but not on normal thymus T lymphomas (0/2) or on rabbit or mink cells infected with BALB/c xenotropic virus. Preincubation of spleen cells with anti-gp70 antiserum inhibited the mitogenic effect of anti-FLV but not of lipopolysaccharide.
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PMID:Antibody directed against Friend leukemia virus stimulates DNA synthesis in a subpopulation of mouse B lymphocytes. 696 99

Nitric oxide (NO) exerts microbicidal effects on a broad spectrum of pathogens, including viruses, but its antiretrovirus properties have not yet been described. The purpose of this study was to determine whether NO inhibits murine Friend leukemia virus (FV) replication in vitro and to what extent NO may play a role in defenses against FV infection in mice. Three NO-generating compounds were studied: 3-morpholino-sydononimine (SIN-1), sodium nitroprusside (SNP), and S-nitroso-N-acetylpenicillamine (SNAP). The effects of these three compounds were compared with those of their controls (SIN-1C, potassium ferricyanide, and N-acetylpenicillamine, respectively), which do not generate NO and with that of sodium nitrite (NaNO2). SIN-1, SNP, and SNAP inhibited FV replication in dunni cells in a concentration-dependent manner. In contrast, no significant inhibitory effect was observed with the three controls or NaNO2. Furthermore, the addition of superoxide dismutase did not alter the inhibitory effect of SIN-1, which is also known to generate superoxide anions. No dunni cell toxicity was observed in the range of concentrations tested. We also assessed the effect of NO produced by activated macrophages on FV replication. Macrophages activated by gamma interferon and lipopolysaccharide inhibited FV replication in a concentration-dependent manner. This inhibition was due in part to NO production, since it was reversed by NG-monomethyl L-arginine, a competitive inhibitor of NO synthase. In vivo administration of NG-nitro-L-arginine methyl ester, a competitive inhibitor of NO synthase, significantly increased the viral load in spleen cells of FV-infected mice. These results suggested that NO may play a role in defenses against the murine Friend leukemia retrovirus.
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PMID:Inhibitory effect of nitric oxide on the replication of a murine retrovirus in vitro and in vivo. 747 19

Friend leukemia virus complex (FLC) infection of BALB/c mice causes a rapid, progressive suppression of most immune functions. In the present study, FLC infection resulted in increased induction by bacterial lipopolysaccharide (LPS) of tumor necrosis factor alpha (TNF alpha) but not IL-6. TNF alpha levels were significantly elevated beginning 11 days post infection and increasing levels were measured through day 21. The highest TNF alpha levels in FCL-infected mice were as much as 100-fold higher than in LPS treated non-infected mice. Peak plasma levels of TNF alpha were seen between 1 and 2 hr after LPS induction, as compared to a peak at 1 hr in controls. The ability of LPS to stimulate TNF alpha was concentration dependent over a range of 0.005 to 50 micrograms per mouse. Using anti-TNF alpha antiserum, cytotoxic activity of plasma was shown to be due specifically to TNF alpha. These data suggest that induction of TNF alpha and IL-6 is regulated by different mechanisms in FLC-infected mice.
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PMID:Enhancement of plasma levels of tumor necrosis factor alpha but not interleukin-6 following endotoxin injection of Friend leukemia virus infected mice. 797 91

The recently cloned fli-1 gene is a member of the ets oncogene family that is preferentially expressed in hematopoietic cells. It is a target of dysregulation by Friend leukemia virus insertion and translocation in Ewing's sarcoma and neuroepithelioma. In this report, we have studied the function and regulation of both murine and human fli-1. Analysis of the human and mouse fli-1 proteins showed that fli-1 binds to specific DNA sequences highly related to m-ets-2 binding sites. Methylation protection experiments showed that fli-1 and m-ets-2 contacted the same nucleotides in two different binding sites. The fli-1 protein was shown to be a transcriptional activator in co-transfection studies. Stimulation of murine bone marrow macrophages by mediators of inflammation, such as lipopolysaccharide, phorbol 12-myristate 13-acetate, interleukin-1, and interferon-gamma resulted in the reduced expression of fli-1 mRNA. fli-1 was only expressed in a defined subset of human erythroleukemia cell lines.
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PMID:Characterization of the ets oncogene family member, fli-1. 844 42

It has been documented that the immune function of leukocytes may be markedly suppressed after infection of mice with the murine retrovirus Friend leukemia virus (FLV). Antimicrobial activity of polymorphonuclear neutrophils (PMNs) against Candida albicans is impaired after retrovirus infection of mice, and this occurs as early as 3 days after infection of genetically susceptible BALB/c mice. By 2 weeks after infection, there was essentially very little growth inhibition of C. albicans by PMNs from the FLV-infected mice. However, when bacterial lipopolysaccharide (LPS), a known activator of macrophages and PMNs, was added to PMNs from the FLV-infected mice, anti-C. albicans activity was restored to normal levels. This restoration of anti-C. albicans activity of FLV-infected mouse PMNs was observed after stimulation with as little as 0.01 micrograms of LPS per ml. The data obtained show that the impaired antimicrobial function of PMNs from retrovirus-infected mice can be readily restored by a biological response modifier such as bacterial LPS.
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PMID:Lipopolysaccharide restores anti-Candida albicans growth inhibition activity of polymorphonuclear neutrophils from retrovirus-immunosuppressed mice. 847 14

By employing the specific histone deacetylase inhibitor trichostatin A (TSA), we investigated whether histone acetylation modulates the production of antigen-specific antibodies in murine splenocytes in vitro. TSA caused a marked increase in both anti-sheep red blood cell (SRBC) and anti-trinitrophenyl (TNP) plaque-forming cell (PFC) responses in splenocytes at much lower concentrations than sodium butyrate. It also dose dependently augmented the production of anti-trinitrophenyl antibodies in splenic B cells with a concomitant, moderate increase in the level of histone H4 acetylation. Its optimal concentration for promoting the production of these antibodies was 10 nM. However, to gain such an effect on antibody production, TSA had to be added to cells before Day 2 in culture. Trichostatin C, an analog of TSA and a less potent inducer of Friend leukemia cell differentiation, also increased both the anti-trinitrophenyl PFC response and histone H4 acetylation in B cells, but at higher concentrations than TSA. TSA did not stimulate the production of lipopolysaccharide-induced polyclonal immunoglobulin M in B cells. These results suggest that a moderate increase in histone acetylation may play a significant role in promoting antigen-specific antibody production in B cells.
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PMID:Promotion of antigen-specific antibody production in murine B cells by a moderate increase in histone acetylation. 982 35