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)

A monoclonal antibody is described that was generated by immunizing mice with cultured human blood monocytes. The antibody (27E10) belongs to the IgG1 subclass and detects a surface antigen at Mr 17,000 that is found on 20% of peripheral blood monocytes. The antigen is increasingly expressed upon culture of monocytes, reaching a maximum between days 2 and 3. Stimulation of monocytes with interferon-gamma (IFN-gamma), 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and lipopolysaccharide (LPS) but not with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) increased the 27E10 antigen density. The amount of 27E10-positive cells is not or is only weakly affected. The antigen is absent from platelets, lymphocytes, and all tested human cell lines, yet it cross-reacts with 15% of freshly isolated granulocytes. By using the indirect immunoperoxidase technique, the antibody is found to be negative on cryostat sections of normal human tissue (skin, lung, and colon) and positive on only a few monocyte-like cells in liver and on part of the cells of the splenic red pulp. In inflammatory tissue, however, the antibody is positive on monocytes/macrophages and sometimes on endothelial cells and epidermal cells, depending on the stage and type of inflammation, e.g., BCG granulomas are negative, whereas psoriasis vulgaris, atopic dermatitis, erythrodermia, pressure urticaria, and periodontitis contain positively staining cells. In contact eczemas at different times after elicitation (6 hr, 24 hr, and 72 hr), the 27E10 antigen is seen first after 24 hr on a few infiltrating monocytes/macrophages, which increase in numbers after 72 hr. From this it is concluded that the antibody 27E10 detects an antigen expressed by a subset of peripheral blood monocytes. In situ the antigen is found only in inflammatory tissues and is absent from normal resident mononuclear phagocytes.
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PMID:A monoclonal antibody to a subset of human monocytes found only in the peripheral blood and inflammatory tissues. 372 15

The regulation of expression of two human granulocyte functional antigens (GFA-1 and GFA-2) was examined. N-formylmethionylleucylphenylalanine (fMet-Leu-Phe) caused a rapid, dose-dependent enhancement of the expression of these antigens, 2- to 4-fold within 30 min, but not of another surface structure, beta 2-microglobulin. Pretreatment of the cells with cytochalasin B at 5 micrograms/ml further enhanced the effect of fMet-Leu-Phe on the expression of GFA-2, raising its surface expression 11-fold. Lipopolysaccharide also stimulated the expression of GFA-1 and GFA-2. The effect of lipopolysaccharide was less than that of fMet-Leu-Phe and was more marked on GFA-1 than on GFA-2. Pretreatment of neutrophils with fMet-Leu-Phe not only stimulated their cytotoxic activity against antibody-coated target cells but also increased their capacity to be stimulated by monoclonal antibodies to GFA-1 and GFA-2. These findings show that the expression of functional surface structures on human neutrophils is subject to rapid and selective regulation.
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PMID:Selective enhancement of the expression of granulocyte functional antigens 1 and 2 on human neutrophils. 388 4

Comparative in vivo and in vitro studies were made on bacterial lipopolysaccharide (LPS) and the chemotactic peptide NF-Met-Leu-Phe with a view toward studying their possible role in the pathophysiology of byssinosis. In contrast to LPS, chemotactic peptides did not cause Limulus amebocyte lysate gelation, nor did they induce the release of endogenous pyrogen. Inhalation of LPS caused a peripheral leukocytosis in rabbits 30 min after aerosol administration, whereas peptide inhalation caused a significant leukopenia in the same period. Cellular analysis of guinea pig bronchial lavages after LPS aerosol challenge revealed immediate decreases in all cell types, with subsequent, large increases of macrophages and granulocytes 4-24 h after aerosolization. Inhalation challenge with NF-Met-Leu-Phe induced no significant cellular changes. It was concluded that it is unlikely that these microbial products could be confused with each other when administered in pure form by the inhalation route.
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PMID:Comparative toxicity studies between bacterial lipopolysaccharide (endotoxin) and N-formyl methionyl peptide as factors in the pathogenesis of byssinosis. 408 22

In vitro antigen-induced tritiated thymidine uptake has been used to study the response of sensitized lymphocytes to (T,G)-A--L, (H,G)-A--L, and (Phe,G)-A--L in responder and nonresponder strains of mice. The reaction is T-cell and macrophage dependent. Highly purified T cells (91% Thy 1.2 positive) are also responsive, suggesting that this in vitro lymphocyte transformation system is not B-cell dependent. Lymphocytes from high and low responder mice stimulated in vitro react as responders and nonresponders in a pattern identical to that seen with in vivo immunization. Stimulation occurs only if soluble antigen is added at physiological temperatures; antigen exposure at 4 degrees C followed by washing and incubation at 37 degrees C fails to induce lymphocyte transformation. Stimulation is specific for the immunizing antigen and does not exhibit the serologic cross-reactivity which is characteristic of these three antigens and their respective antisera. The reaction can be inhibited by anti-H-2 sera but not by anti-immunoglobulin sera. The anti-immunoglobulin sera did, however, inhibit lipopolysaccharide or pokeweed mitogen stimulation. These results suggest that the Ir-1A gene(s) are expressed in T cells, and that there are fundamental physiologic differences between T- and B-cell antigen recognition.
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PMID:Genetic control of the immune response: in vitro stimulation of lymphocytes by (T,G)-A--L, (H,G)-A--L, and (Phe,G)-A--L. 454 82

We investigated the capacity of bacterial endotoxin (lipopolysaccharide, LPS) to modify the oxidative metabolic response to membrane stimulation of human neutrophils. Neutrophils were pretreated for 60 min with LPS, 10 ng/ml, then stimulated by exposure to fixed immune complexes, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP), or phorbol myristate acetate. Release of superoxide anion (O-2) was up to 7-times greater in cells preincubated with LPS, depending upon the stimulus used. Consumption of oxygen and release of hydrogen peroxide (H2O2) were similarly increased, using FMLP as stimulus. The enhancement was accompanied by a reduction in lag time and an increase in the rate of the response, but the duration of the oxidative events was not changed. The molecular basis for the augmented oxidative response of LPS-pretreated cells was investigated. Preincubation with LPS at 0 degrees C prevented priming, but preincubation in the presence of cycloheximide or chelation of extracellular calcium ion did not. Neutrophils preincubated with LPS had slightly decreased numbers of binding sites and equivalent binding affinity for radiolabeled FMLP. Possible changes in the enzyme responsible for the oxidative burst were analyzed by studying NADPH-dependent generation of O-2 by particulate fractions from cells preincubated with LPS or buffer, then stimulated before cell disruption. The fraction prepared from LPS-pretreated neutrophils exhibited greater release of O-2 over a wide range of concentrations of NADPH. The calculated apparent Km for NADPH was equivalent in the two fractions, but the Vmax was increased 2.5-fold in the subcellular fraction from LPS-pretreated cells. These results suggest that LPS could increase neutrophil-mediated host defense or the tissue damage associated with endotoxemia by enhancing the generation of oxygen metabolites by neutrophils. These results also support the concept that the neutrophil is not an end-stage cell in regard to function or metabolic activity.
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PMID:Priming of neutrophils for enhanced release of oxygen metabolites by bacterial lipopolysaccharide. Evidence for increased activity of the superoxide-producing enzyme. 609 75

Although capable of provoking a variety of inflammatory effects, endotoxin (bacterial lipopolysaccharide) paradoxically has been reported to be antiinflammatory. The authors have found that single intravenous injections of Escherichia coli endotoxin, 24 hours before challenge, inhibit almost completely the vascular permeability changes and exudation of polymorphonuclear leukocytes induced in rabbit skin by reversed passive Arthus reactions. Whereas intravenous injections of endotoxin also caused modest inhibition of the vascular permeability changes induced in rabbit skin by the synthetic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP), exudation of polymorphonuclear leukocytes was unaffected. Polymorphonuclear leukocytes from rabbits given single injected doses of endotoxin exhibited markedly diminished chemotactic and degranulation responses to complement (C5)-derived peptides in vitro. Responses of these cells to FMLP, however, were normal. These data suggest that selective suppression of polymorphonuclear leukocyte responses to C5-derived peptides accounts, in part, for the antiinflammatory effects of endotoxin.
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PMID:Antiinflammatory effects of endotoxin. Inhibition of rabbit polymorphonuclear leukocyte responses to complement (C5)-derived peptides in vivo and in vitro. 622 51

The secretion of the phospholipase A2-inhibitor macrocortin and the binding of dexamethasone were studied in suspensions of rat peritoneal macrophages. Corticosteroid-induced macrocortin secretion was specific for glucocorticoids and did not occur in response to glucocorticoid antagonists or other steroids or in response to non-steroid macrophage activators (formyl-methionyl-leucyl-phenylalanine f-MLP), the calcium ionophore A23187, phorbol myristate acetate (PMA) and lipopolysaccharide-E.-coli(LPS) ). The apparent potency of competition by secretory glucocorticoids for dexamethasone binding to the macrophage parallelled their ability to induce secretion, implying that these binding sites represent the receptors by which macrocortin secretion is initiated. Agents which interfere with microtubule assembly (colchicine, vinblastine and trimethylcolchicinic acid) and prostacyclin and dibutyryl cyclic AMP inhibit macrocortin secretion. Inhibition studies of glucocorticoid-induced macrocortin secretion also suggest dependence upon metabolic energy, a source of Ca2+ and proteolysis and glycosylation prior to secretion.
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PMID:Specificity and inhibition of glucocorticoid-induced macrocortin secretion from rat peritoneal macrophages. 631 16

A precise method for quantitation of polymorphonuclear leukocyte (PMNL) accumulation in skin in vivo, has been developed so that the proinflammatory effects of various agents can be compared. This method can also be used to evaluate the effect of therapeutic agents on PMNL accumulation in vivo. Rabbit PMNLs were purified from heparinized blood by dextran sedimentation, hypotonic lysis, and separation on Ficoll-Hypaque. The PMNLs were labeled with 3-5 microCi per 10(6) cells of 111In oxine and reinfused coincidentally with different concentrations of different chemotactic and proinflammatory materials injected intradermally into the back. In some experiments, varying concentrations of acetic acid were applied topically. Four to 18 hours later, the rabbits were sacrificed. Eight-millimeter punch biopsies were obtained from the injection sites and counted in a gamma counter. The number of PMNLs infiltrating the dermis was also quantitated in histologic sections. A significant correlation was found between the percent increase in radioactivity and the percent increase in PMNL accumulation morphologically. Dose-response curves were generated using such proinflammatory materials as formyl-methionyl-leucyl-phenylalanine, lipopolysaccharide, activated serum, trypsin, glycogen, and acetic acid. These curves were highly reproducible from animal to animal. Using this assay, we found that as little as 1 microgram of trypsin induced detectable PMNL accumulation. This is 2-3 logs more sensitive than injecting mice intraperitoneally with trypsin. Diisopropyl fluorophosphate-inactivation of trypsin inhibited PMNL accumulation. This sensitive and quantitative bioassay of PMNL accumulation permits evaluation of multiple agents in the same animal, which decreases animal to animal variation.
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PMID:Labeling of peripheral blood polymorphonuclear leukocytes with indium-111: a new method for the quantitation of in-vivo accumulation of PMNLs in rabbit skin. 642 Apr 76

The effect of graded amounts of dietary lactalbumin (L) and casein (C) hydrolyzates on the immune responsiveness of C3H/HeN and DBA/2 strain mice has been investigated by measuring both the specific humoral immune response to sheep red blood cells (SRBC) and the nonspecific splenic cell responsiveness to phytohemagglutinin, concanavalin A and Escherichia coli lipopolysaccharide after stimulation with Mycobacterium bovis, strain BCG. The nutritional efficiency of these diets was similar at both 12 and 28% amino acid levels. The immune responses of mice fed the L diets were found to be significantly greater than those of mice fed the corresponding C diets, especially at the 28% level. Furthermore in the mice fed L diet, increasing the concentration of amino acid in the diet from 12 to 28% greatly enhanced immune responsiveness by both parameters measured. In the C-fed mice, a comparable enhancement of mitogen responsiveness with increasing amino acid level of diet was seen, but there was no change in the humoral immune response. The enhancement of immune responsiveness observed in mice fed the 28% L diet was moderately reduced by the addition of phenylalanine to the diet, indicating that the lower level of this amino acid in the L protein may be of some significance. These dietary effects on immune responsiveness were remarkably similar in both mouse strains tested.
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PMID:Influence of dietary proteins on the immune system of mice. 705 Mar 21

Because a general study of activated neutrophils may have relevance to periodontal diseases and accompanying inflammation, we studied a function of mouse polymorphonuclear leukocytes (PMNs) that exude into the peritoneal cavity in response to inflammation caused by i.p. injection of 2% casein. The effects of E. coli-lipopolysaccharide (E-LPS) and a chemotactic factor, N-formyl-N-methionyl-N-leucyl-L-phenylalanine (FMLP), on the level of intracellular calcium ([Ca2+]i) in these PMNs were examined. From analysis made with a laser cytometer (ACAS 570), the PMNs in exudates harvested 3-9 h after the onset of inflammation were shown to undergo [Ca2+]i elevation in response to 10(-6) M FMLP. The peak concentration of [Ca2+]i elicited by FMLP was highest in exudate cells 6 h after casein injection. In addition, about 65% of the PMNs in the 3-h exudate were FMLP sensitive displaying an elevated [Ca2+]i, whereas more than 85% of them in 6- and 9-h exudates became FMLP sensitive. Also, the maximum level of [Ca2+]i after FMLP stimulation was potentiated by pretreatment of the cells with E-LPS (0.2 microgram/ml). The present study suggests that PMNs induced by casein injection and appearing in mouse peritoneal exudate at different times possess significantly different ability to undergo [Ca2+]i elevation, and different susceptibility toward a chemotactic factor, FMLP.
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PMID:Effects of FMLP and LPS on [Ca2+]i of peritoneal exudate polymorphonuclear leukocytes following onset of inflammation. 747 96


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