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)

Histamine and putrescine (a precursor of polyamines) are formed by histidine decarboxylase (HDC) and ornithine decarboxylase (ODC), respectively. Within a few hours after injection of a lipopolysaccharide (LPS) into mice, HDC is induced in the liver, spleen, lung and bone marrow, and ODC is induced in the liver, spleen and bone marrow. Since LPS is known to stimulate the production of various cytokines, the abilities of various cytokines to induce HDC and ODC in the tissues of mice were examined. IL-2, IL-6, IL-8, IFN gamma and M-CSF were ineffective. IL-1 alpha, IL-1 beta, TNF alpha and TNF beta induced HDC and ODC, as does LPS. On the other hand, GM-CSF and G-CSF induced HDC and ODC only in the spleen and bone marrow within a few hours after their injection. These results suggest that, in addition to their roles in inflammation or immune responses, HDC and ODC are also involved in an early stage of hematopoiesis.
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PMID:GM-CSF and G-CSF stimulate the synthesis of histamine and putrescine in the hematopoietic organs in vivo. 138 20

Histamine release caused by calcium ionophore A23187 and anti-IgE was examined in leukocyte suspensions from 8 healthy individuals. Staphylococcus aureus, lipopolysaccharide (LPS) from Salmonella typhimurium and influenza A virus were found to enhance the histamine release but did not release histamine per se. The potentiation of mediator release depends on a non-transient signal since the potentiating effect was also obtained by preincubation of the cells with LPS followed by wash-out and stimulation of the cells with anti-IgE. The potentiation was abolished or reduced by galactose, N-acetyl-glucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. These findings indicate that the enhancement of mediator release by bacteria, endotoxin, and virus depends on a sugar-mediated reaction.
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PMID:Carbohydrates inhibit the potentiating effect of bacteria, endotoxin and virus on basophil histamine release. 169 60

Histamine release from human basophil leukocytes from allergic patients or controls was induced by specific antigens, anti-IgE or calcium ionophore A23187. Influenza A virus, S. aureus and lipopolysaccharide from S. typhimurium increased the maximum release of histamine and caused a shift to the left of the dose-response curves showing increased cell sensitivity and lowering of the threshold to these stimuli. The mechanism of action was elucidated by examining the mediator release as a function of increasing extracellular concentration of calcium. In these experiments the dose-response curves were changed by the microorganisms and lipopolysaccharide as before. This indicates that the microorganisms and lipopolysaccharide change the basophil cell response to IgE-dependent and non-immunological stimuli by causing a change in the subcellular handling of calcium.
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PMID:Virus, bacteria and lipopolysaccharide increase basophil cell response to histamine releasing stimulators and calcium. Examination of allergic and normal individuals. 171 94

This study was aimed at evaluating the effect of histamine on tumor necrosis factor (TNF alpha) secretion by purified human blood monocytes. TNF alpha was measured by radioimmunoassay. Histamine caused a dose-dependent inhibition of lipopolysaccharide-induced TNF alpha production from human blood monocytes, averaging maximally 50% at 10(-5) M. Preincubation of mononuclear cells with an H2 antagonist (cimetidine), but not with an H1 antagonist (promethazine) prevented this inhibitory effect of histamine. In conclusion, histamine causes, in vitro, a depression of TNF alpha secretion by human monocytes through activation of H2 receptors.
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PMID:Effect of histamine on tumor necrosis factor production by human monocytes. 193 30

Histamine-releasing effect of polymyxin B1 and its deacylated analogues has been studied on purified rat mast cells. The structure-activity analysis showed that cyclic peptide fragment and acyl residue of molecule of polymyxin plays an important role in histamine-releasing activity. Histamine release, induced by polymyxin B1 and its analogue was blocked by metabolic inhibitor antimycin A. Preincubation of polymyxin B1 with lipopolysaccharide inhibits in dose-dependent manner polymyxin-induced histamine secretion from rat mast cells.
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PMID:[The histamine-liberating action of polymyxin B and its analogs]. 247 Apr 41

When spleen cells of C57BL/6 mice or mast cell-deficient W/Wv mice were cultured, their histidine decarboxylase (HDC) activity increased with increases in the histamine concentration in the cells and the medium. Addition of concanavalin A (Con A) or Escherichia coli lipopolysaccharide (LPS) enhanced the increase. The removal of adherent cells reduced both the control HDC activity and the response to the mitogens. Purified T lymphocytes responded to Con A but not to LPS. Neither Con A nor LPS had any effect on B lymphocytes. Treatment of T cells with anti-Thy-1.2 and complement completely abrogated the induction of HDC. Histamine synthesis dependent on Con A by T cells was stimulated by the addition of conditioned medium from peritoneal adherent cells activated with LPS. The addition of recombinant interleukin-1 (rIL-1) or peritoneal adherent cells fixed with paraformaldehyde significantly enhanced HDC induction dependent on Con A in T cells. These results suggest that histamine is synthesized by T lymphocytes through HDC and that the reaction was enhanced by a soluble factor(s) released from macrophages.
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PMID:Histamine synthesis by mouse T lymphocytes through induced histidine decarboxylase. 278 10

Histamine inhibited the production of interleukin 1 (IL-1) induced by lipopolysaccharide (LPS) in cultures of purified human peripheral blood monocytes. The effect of histamine on IL-1 production was dose-dependent and significant at histamine concentrations of 10(-4)-10(-5) M. The histamine H2 receptor agonists dimaprit and 4-methylhistamine, but not the H1 receptor agonists 2-pyridylethylamine, aminoethylthiazole and 2-methylhistamine, modulated the IL-1 production in a similar manner to histamine. The inhibitory effects of histamine could be reversed by the H2 receptor antagonist cimetidine but not by the H1 receptor antagonist mepyramine. This indicates that the inhibitory effects of histamine on LPS-induced IL-1 production are mediated through H2 receptors on human peripheral blood monocytes.
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PMID:Histamine inhibits interleukin 1 production by lipopolysaccharide-stimulated human peripheral blood monocytes. 289 11

When cells of mouse myelomonocytic leukemia cell line, WEHI-3B, were cultured in the presence of actinomycin D plus the serum which was obtained from mice injected with bacterial endotoxin, i.e., lipopolysaccharide, their histidine decarboxylase (L-histidine carboxy-lyase, EC 4.1.1.22) (HDC) activity increased about 100-fold with a peak at 48 h. According to the increase in HDC activity, the expression of surface antigens associated with macrophages, such as Mac II, Mac III and Iad, increased markedly on WEHI-3B cells as well as their morphological changes to macrophages. Histamine levels in the culture medium increased concomitantly with the increase in the HDC activity in WEHI-3B cells, whereas the histamine contents inside the cells did not increase remarkably. Furthermore, the addition of lipopolysaccharide to the culture medium caused an additional 2-fold increase in the HDC activity of WEHI-3B cells. These results indicate that the increase in HDC activity in WEHI-3B cells may represent an event in the process of the differentiation to macrophages.
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PMID:Increase of histidine decarboxylase activity in murine myelomonocytic leukemia cells (WEHI-3B) in parallel to their differentiation into macrophages. 305 14

This study was carried out on the effect of histamine hydrochloride and its antagonists on the production of interleukin-1 (IL-1) by lipopolysaccharide (LPS)-stimulated adherent human monocytes (AHM) from normal healthy blood donors. IL-1 activity was evaluated by incorporation of [3H]-thymidine in mouse thymocytes in samples of 1:3 dilution. The result indicated that histamine hydrochloride significantly suppressed IL-1 production by AHM at 10(-3) M and 10(-10) M in 14 donors with maximal suppression observed at 10(-3) M. A 1-hr incubation with histamine hydrochloride (10(-3) M) before addition of LPS was found to be appropriate. Cimetidine, an H2-antagonist at 10(-3) M, 10(-5) M, and 10(-7) M significantly inhibited the effect of histamine hydrochloride (10(-3) M) and gave maximum inhibition at 10(-5) M, whereas chlorpheniramine maleate, and H1-antagonist had no significant inhibitory effect at the concentrations studied (10(-4) M, 10(-5) M, and 10(-7) M). Histamine hydrochloride (10(-3) M) added alone had no significant suppressive effect, while cimetidine (10(-5) M) alone had a significant stimulatory effect on IL-1 production by AHM.
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PMID:Effect of histamine and antihistamines on interleukin-1 production by human monocytes. 350 82

The induction of macrophage procoagulant activity by specific antigens is a close in vitro correlate of delayed-type hypersensitivity (DTH) reactions and provides a quantitative and sensitive measure of cell-mediated immune responses. The reaction is mediated by lymphokines from activated T lymphocytes and is potentiated by bacterial lipopolysaccharide. Lymphokines directly activated procoagulant activity on some murine and human macrophage tumor cell line cells although others required the collaboration of T lymphocytes, in the presence of lymphokine, to express activity. Macrophages in different stages of differentiation may vary, therefore, in their response to lymphokines. Pharmacological agents which regulate DTH reactions also mediated either the ability of lymphocytes to produce macrophage procoagulant inducing factor or the response of macrophages to the factors. Histamine and an anticoagulant found on stimulated T lymphocytes may be important regulatory mediators of macrophage procoagulant activity in vivo.
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PMID:Induction of macrophage procoagulant by products of activated lymphocytes. 639 41


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