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)

Peripheral blood B-lymphocyte markers and functions were observed in 21 patients with IgA nephropathy (IgA NP), 18 patients with systemic lupus erythematosus (SLE) and 16 controls. IgA NP B-lymphocytes similarly to that of SLE B-lymphocytes expressed significantly higher positivity with Leu 1 (CD 5) monoclonal antibody than controls. CD 5 positive B-lymphocytes are thought to be a distinct subset of the B-cells (autoregulatory B-lymphocytes) inducible in IgA NP by lipopolysaccharide (LPS) stimulation in parallel to their expression of surface IgM heavy chain positivity. The activated state of IgA NP B-lymphocytes have been proved by their higher OKIa (HLA-DR) positivities but lower IOB1a (CD 21, C3b-receptor) and decreased IgG-Fc-receptor (ox- rosette) expression. IgA NP B-lymphocytes showed a higher IgA but also IgG and IgM polyclonal immunoglobulin production than control B-lymphocytes in co-cultures with T-lymphocytes. Not only regulatory T-lymphocyte subsets but also serum derived from IgA NP patients stimulated the immunoglobulin production of IgA NP B-lymphocytes.
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PMID:[Markers of peripheral B lymphocytes and their function in IgA nephropathy]. 220 18

We investigated the effects of recombinant C5a (rC5a) on gene expression and synthesis of interleukin-1 beta (IL-1 beta) and tumor necrosis factor (TNF) in fresh human peripheral blood mononuclear cells (PBMC). Total (cell-associated and secreted) cytokine synthesis was measured. In the strict absence of endotoxin (lipopolysaccharide [LPS]), rC5a resulted in a small but statistically insignificant increase in immunoreactive IL-1 beta and TNF, as well as in IL-1 and IL-6 bioactivity. On the other hand, rC5a induced marked transcriptional activation of IL-1 beta and TNF in a dose-dependent fashion with an optimal concentration of 50 ng/mL. The rC5a-induced cytokine messenger RNA (mRNA) was not spontaneously translated into protein. At 50 ng/mL, rC5a induced the same levels of mRNA for IL-1 beta and TNF as 1 ng/mL of LPS, whereas LPS induced 12 times more IL-1 beta protein and 70 times more TNF protein than rC5a alone. The C5a-induced mRNA half-life was the same as that induced by LPS. Formyl-Meth-Leu-Phe (fMLP) did not induce cytokine transcription. Pretreatment with rC5a enhanced cytokine synthesis induced by other stimuli. After 2 hours of preincubation with rC5a, PBMC synthesized 3 to 10 times more IL-1 beta and TNF on subsequent stimulation by LPS or IL-1 itself. We conclude that rC5a provides primarily a transcriptional but not translational signal for IL-1 beta and TNF; the half-life of the untranslated mRNA is the same as that of translated message; rC5a-induced transcription upregulates PBMC for enhanced synthesis of these cytokines; and a translational signal can be provided by LPS or IL-1 itself.
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PMID:Recombinant C5a stimulates transcription rather than translation of interleukin-1 (IL-1) and tumor necrosis factor: translational signal provided by lipopolysaccharide or IL-1 itself. 220 33

The product of the human GRO gene is a cytokine with inflammatory and growth-regulatory properties; GRO is also called MGSA for melanoma growth-stimulatory activity. We have identified two additional genes, GRO beta and GRO gamma, that share 90% and 86% identity at the deduced amino acid level with the original GRO alpha isolate. One amino acid substitution of proline in GRO alpha by leucine in GRO beta and GRO gamma leads to a large predicted change in protein conformation. Significant differences also exist in the 3' untranslated region, including different numbers of ATTTA repeats associated with mRNA instability. A 122-base-pair region in the 3' region is conserved among the three GRO genes, and a part of it is also conserved in the Chinese hamster genome, suggesting a role in regulation. DNA hybridization with oligonucleotide probes and partial sequence analysis of the genomic clones confirm that the three forms are derived from related but different genes. Only one chromosomal locus has been identified, at 4q21, by using a GRO alpha cDNA clone that hybridized to all three genes. Expression studies reveal tissue-specific regulation as well as regulation by specific inducing agents, including interleukin 1, tumor necrosis factor, phorbol 12-myristate 13-acetate, and lipopolysaccharide.
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PMID:Identification of three related human GRO genes encoding cytokine functions. 221 7

The nature of endogenous acceptor molecules implicated in the membrane-directed synthesis of the polysialic acid (polySia) capsule in Escherichia coli K1 serotypes is not known. The capsule contains at least 200 sialic acid (Sia) residues that are elongated by the addition of new Sia residues to the nonreducing termini of growing nascent chains (Rohr, T. E., and Troy, F. A. (1980) J. Biol. Chem. 255, 2332-2342). Presumably, chain growth starts when activated Sia residues are transferred to acceptors that are not already sialylated. In the present study, we used an acapsular mutant defective in synthesis of CMP-NeuAc to label acceptors with [14C]NeuAc and an anti-polySia-specific antibody (H.46) to identify the molecules to which the polySia was attached. [14C]Sia-labeled acceptors were solubilized with 2% Triton X-100, immunoprecipitated with H.46, and partially depolymerized with poly-alpha-2,8-endo-N-acetylneuraminidase. Approximately 5% of the [14C]Sia incorporated remained attached to endogenous acceptors. Double-labeling experiments were used to show that the non-Sia moiety of the acceptor was labeled in vivo with [14C]leucine and elongated in vitro with CMP-[3H]NeuAc. Concomitant with desialylation of the [3H]polySia-[14C]Leu acceptor was the appearance of a new [14C]Leu-labeled protein at 20 kDa. After strong acid hydrolysis, the 20-kDa labeled protein was shown to contain [14C]Leu. The acceptor molecules were not labeled metabolically with D-[3H]GlcN, 35SO4, or 32PO4, indicating that they do not appear to contain lipopolysaccharide, peptidoglycan, phosphatidic acid, or phospholipid. Based on these results, we conclude that the endogenous acceptor molecule is a membrane protein of about 20 kDa. The nature of attachment of polySia to acceptor is unknown. There are only 400-500 acceptor molecules/cell, which is about 100-fold fewer than the 50,000 polySia chains/cell. This suggests that each acceptor molecule may participate in the shuttling of about 100 polySia chains/cell. We hypothesize that the acceptor protein may function to translocate polySia chains from their site of synthesis on the cytoplasmic surface of the inner membrane to the periplasm.
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PMID:Biosynthesis of the polysialic acid capsule in Escherichia coli K1. The endogenous acceptor of polysialic acid is a membrane protein of 20 kDa. 240 16

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

SDS-PAGE analysis of plasma samples from mice injected with high, but nontoxic, concentrations of indomethacin led to the detection of elevated levels of a 125,000 dalton protein. The appearance of this protein was rapid, occurring within 24 hrs after a single injection of the drug. Treatment of mice with similar concentrations of sulindac and derivatives, the indomethacin analogs MK-410 and MK-555, or high doses (1 mg/day) of aspirin, did not induce the appearance of this protein. However, the appearance of this protein was rapidly induced by inflammatory agents such as turpentine or bacterial lipopolysaccharide. In addition, the protein was induced by RES stimulating agents such as C. parvum and BCG but it was not induced in tumor-bearing animals with activated RE systems. Administration of [3H]-leucine to animals treated with indomethacin, turpentine or lipopolysaccharide revealed the accelerated synthesis of primarily the 125 kilodalton protein but also the synthesis of several other plasma proteins as well. These results indicate that treatment of mice with indomethacin uniquely induces changes in plasma proteins with the characteristics of an acute phase response. This ability of indomethacin may reside in its ability to activate murine macrophages.
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PMID:Treatment of mice with indomethacin leads to the appearance of a 125,000 dalton plasma protein with the characteristics of an acute phase reactant. 244 92

We have previously shown that peripheral blood natural killer (NK) cells have significant levels of cytotoxic activity against Shigella flexneri-infected HeLa cells. In this report, we show that NK cell activity against K562 tumor cells and Shigella flexneri-infected HeLa cells can be greatly enhanced by preincubating peripheral blood lymphocytes (PBL) for 18 h with kanamycin-treated Shigella flexneri or Salmonella typhimurium. Cell-free supernatants obtained from PBL-bacteria cultures contained high levels of interferon (IFN) activity, which was characterized as a mixture of IFN-gamma and IFN-alpha. Cytotoxic activity associated with PBL precultured with shigellae was associated with predominantly CD16+ (Leu-11+) and CD2+ (OKT-11+) cells. Further, IFN production was dependent upon the presence of CD16+ and CD2+ cells at culture initiation. Enhancement of cytotoxic activity associated with PBL-bacteria cultures did not, however, appear to be dependent upon IFN production, since low numbers of bacteria which failed to stimulate IFN production induced high levels of NK cell activity. Lipopolysaccharide appeared not to be involved in bacteria-induced IFN production or enhanced NK cell activity, since Salmonella lipopolysaccharide failed to induce IFN production or enhance NK cell activity. These results suggest that IFN production by NK cells and the killing of bacteria-infected cells play an important role in host defense against facultative intracellular bacterial infections.
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PMID:Natural killer cell activation and interferon production by peripheral blood lymphocytes after exposure to bacteria. 245 65

The fibrinolytic potency of several polyanions was comparatively investigated. Fibrinolytic activity was measured in a whole plasma assay using H-D-Val-Leu-Lys-pNA (S-2251) as chromogenic substrate and by a fibrin plate assay using plasminogen rich fibrin plates. In the chromogenic substrate assay potent fibrinolytic polyanions comprised dextran sulfate, GAGPS, pentosan polysulfate, polyanethol sulfate, l-carrageenan and i-carrageenan. Chondroitin sulfates A, B, C, keratan sulfate, ribonucleic acid, k-carrageenan and heparin were weakly fibrinolytic. Hyaluronic acid and lipopolysaccharide from E. coli were inactive. Similar results were obtained when fibrinolytic activity was measured by a fibrin plate assay. All polyanions except lipopolysaccharide produced lysis zones. Induction of fibrinolytic activity in human plasma was shown to be at least partially dependent on Hageman factor. In factor XII deficient plasma no fibrinolysis was induced by any of the polyanions when measured in the fibrin plate assay. In the chromogenic substrate assay corn Hageman factor inhibitor (CHFI) inhibited the activation of S-2251 cleaving enzyme by GAGPS, pentosan polysulfate, polyanethol sulfate, heparin, and ribonucleic acid near completely. The activation by dextran sulfate was inhibited by 45%. Heparin, pentosan polysulfate and GAGPS, three polyanions of therapeutic interest were separately compared. In both assays GAGPS proved the most potent activator, while pentosan polysulfate exhibited 83% and 44% and heparin 32% and 14% of GAGPS fibrinolytic activity in the chromogenic substrate test and the fibrin plate assay, respectively.
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PMID:Induction of fibrinolysis by polyanions in human plasma. 246 1

M1 cells derived from mouse myeloid leukemia have been reported to differentiate to macrophage-like cells upon treatment with substances such as lipopolysaccharide. Previously we found that in mouse peritoneal macrophages most of the neutral amino acids were taken up through a unique Na+-independent system. In this paper we have investigated the neutral amino acid transport in M1 cells and in those treated with lipopolysaccharide. In M1 cells serine, alanine and proline were taken up mainly by Na+-dependent transport systems, and leucine was largely transported by a Na+-independent system. By treating the cells with lipopolysaccharide, the activities of the Na+-dependent systems markedly decreased, whereas the activity of the Na+-independent system was little affected. The amino acid concentrations in the cells and the culture medium were measured. As a whole, the intracellular to extracellular distribution ratios for neutral amino acids that are preferred substrates for Na+-dependent systems were decreased on lipopolysaccharide treatment, whereas those for amino acids that are mainly transported by a Na+-independent system were slightly increased. From these results we conclude that M1 cells treated with lipopolysaccharide tend to differentiate to macrophage-like cells with respect to the neutral amino acid transport.
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PMID:Changes in neutral amino acid transport activity in myeloid leukemia cells differentiated by lipopolysaccharide. 250 38

Plasma endotoxin concentrations and oxidative burst response of peripheral blood polymorphonuclear leukocytes were examined in 12 patients undergoing coronary artery bypass. The measurements were made just before the operation, 5 minutes after removal of the aortic crossclamp, and 24 hours after the operation. Endotoxin was quantitated by a combination of a sensitive Limulus amebocyte lysate assay and rocket immunoelectrophoresis measuring picogram amounts of endotoxin. Peripheral blood neutrophils were purified by a two-step dextran sedimentation and metrizoate sodium Ficoll (Lymphoprep., Nyegaard, Oslo, Norway) centrifugation. The oxidative burst response of these cells was measured for their ability to generate superoxide anion and was determined by a cytochrome c reduction assay. Preoperatively, all the plasma samples except one were free of endotoxin. The endotoxin levels reached 100 pg/ml 5 minutes after removal of the aortic crossclamp, and except in one sample they had decreased 24 hours after the operation. Studies on the generation of superoxide by neutrophils showed a decline in the response 5 minutes after removal of the aortic crossclamp and an enhancement of the response to f-Met-Leu-Phe by cells obtained from 11 of 12 patients 24 hours postoperatively. In vitro addition of bacterial lipopolysaccharide to blood from healthy individuals also enhanced the superoxide response of the neutrophils. We conclude that during cardiopulmonary bypass the circulating blood is contaminated by endotoxin and the neutrophils are primed for enhanced generation of oxygen radicals. The released oxygen radicals may be involved in the tissue damage observed in these patients.
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PMID:Endotoxemia and enhanced generation of oxygen radicals by neutrophils from patients undergoing cardiopulmonary bypass. 254 7


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