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)

Escherichia coli lipopolysaccharide (LPS) induced a strong secretion of corticosterone in C3H/HeN mice with a concomitant increase in the splenic histidine decarboxylase activity. Treatment of the mice with alpha-fluoromethyl histidine, a suicide substrate for the enzyme, markedly attenuated both the secretion and the increase. In C3H/HeJ mice, LPS provoked little corticosterone release and induction of the enzyme. However, these mice responded to tetradecanoyl phorbol acetate with a large increase in both this secretion and enzyme activity. Injection of LPS produced a comparable increase in the serum histamine and corticosterone level and activity of histidine decarboxylase in various tissues of genetically mast-cell-deficient W/WV mice and in closely related +/+ mice. These results suggest that secretion of corticosterone caused by LPS is mediated by histamine produced through induction of histidine decarboxylase in non-mast cells.
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PMID:Possible role of endogenous histamine in mediation of LPS-induced secretion of corticosterone in mice. 375 16

Mice were injected intraperitoneally with 50 mug of Escherichia coli lipopolysaccharide (LPS). The spleen tissue exhibited increased histamine-forming capacity (HFC) 4 hr later. When this increased HFC was produced within 12 hr after intraperitoneal injection of sheep red blood cells (SRBC), there was an enhanced anti-SRBC antibody response in the spleen. In mice experiencing an increased spleen HFC at 36 hr after injection of SRBC, there was a significant decrease in the number of antibody-producing cells. The injection of histidine decarboxylase inhibitors simultaneously with the LPS greatly reduced the stimulation of HFC and also the adjuvant activity of the LPS.
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PMID:Influence of Escherichia coli lipopolysaccharide on histamine-forming capacity and antibody formation in lymphoid tissues. 494 1

Various types of mitogenic substances, such as a Escherichia coli lipopolysaccharide (LPS), concanavalin A (Con A), pokeweed mitogen, polyI:polyC (a synthetic double-stranded RNA) and 12-O-tetradecanoylphorbol-13-acetate (a component of croton oil), induced histidine decarboxylase (HDC) in the liver, spleen and lung of mice at 4.5 hr after injection. Other inflammatory agents without mitogenic activity, such as zymosan, carrageenan, glycogen, D-galactosamine and N-acetyl-muramyl-L-alanyl-D-isoglutamine, did not induce the enzyme. Both LPS (a B-cell mitogen) and Con A (a T-cell mitogen) induced HDC also in nude mice that lack T-cells, indicating that T-cells are not required for HDC induction by mitogens. C3H/HeJ mice, which are LPS-low responder mice in various immunological tests, were quite a bit less responsive to LPS also in the HDC induction. These results show that mitogens with different properties can induce HDC as a common characteristic. On the basis of these results, the possible participation of macrophages in the process of HDC induction by mitogens was discussed.
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PMID:Induction of histidine decarboxylase in mouse tissues by mitogens in vivo. 666 Dec 56

The injection of Escherichia coli lipopolysaccharide (LPS) into mice produced simultaneous induction of histidine and ornithine decarboxylases in the liver, lung, spleen and kidney. The time courses of the changes in activities of the two enzymes were similar in all the tissues. After the injection, both activities increased within 1.5 hr, peaked at 4.5 hr and returned to the basal levels within 15 hr. The induction of these enzymes was very sensitive to this agent, i.e. as little as 1 microgram/kg of the E. coli lipopolysaccharide produced significant increases in these enzyme activities. An increase in the product amines, histamine and putrescine, followed the rise of enzyme activities. The levels of histamine changed more rapidly than those of putrescine. In spite of the increase in putrescine, there was no increase in spermidine and spermine. In the brain and thymus the LPS induced ornithine decarboxylase, but not histidine decarboxylase. In the blood, the histamine level increased without an increase in the activity of histidine decarboxylase. These results are discussed in relation to the actions of lipopolysaccharide. A simple method for the simultaneous assay of the activities of histidine and ornithine decarboxylases without using radioisotope substrates was used in this study.
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PMID:Simultaneous induction of histidine and ornithine decarboxylases and changes in their product amines following the injection of Escherichia coli lipopolysaccharide into mice. 704 56

We have previously demonstrated the increase of histidine decarboxylase activity and histamine content in the murine hypothalamus after intracerebroventricular injection of lipopolysaccharide possibly due to inducible interleukin-1 beta (IL-1 beta). Therefore, we investigated the effects of IL-1 beta on brain histamine dynamics by directly injecting it into the tuberomammillary nucleus of the rat hypothalamus (TM) using an in vivo microdialysis method. Injection of artificial cerebrospinal fluid or recombinant murine IL-1 beta at 0.1 ng into the TM did not evoke a significant change in core temperature, however, a significant monophasic febrile response was observed following injection of IL-beta at more than 1 ng per animal. Histamine release in the anterior hypothalamic area in vivo was significantly augmented from 140 min to 360 min following injection of IL-1 beta at 10 ng dose. These results suggest the possibility that interrelationship between histamine and IL-1 beta may modulate the acute phase reaction in the central nervous system.
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PMID:Interleukin-1 beta induces histamine release in the rat hypothalamus in vivo. 753 93

An injection of Escherichia coli lipopolysaccharide (LPS) increased the activity of histidine decarboxylase (HDC) in bone marrow (BM) cells of C3H/HeN mice much more than in C3H/HeJ mice, which are resistant to various effects of LPS. In WBB6/F1 (W/Wv) mice, which are genetically deficient in mast cells, HDC activity increased more than in C3H/HeN mice. Cultured BM cells of W/Wv mice spontaneously synthesized histamine in a HDC-dependent way. LPS caused a slight increase in HDC-associated histamine synthesis by these cells. Treatment of the BM cells with murine recombinant granulocyte-macrophage colony stimulating factor (mrGM-CSF) increased the histamine synthesis. In addition, treatment with mrGM-CSF made the cells respond to LPS by a dose-dependent increase in HDC activity and histamine synthesis. Most dish-adherent BM cells that had been treated with both mrGM-CSF and LPS for 48 h were stained for nonspecific esterase and not for chloroacetate esterase, and had twice as much HDC activity as the nonadherent cells had. Immunocytochemical analysis of the BM cells of W/Wv mice treated with both mrGM-CSF and LPS showed that HDC was in the cytoplasm of cells having Mac-1, a macrophage-differentiation antigen. These results suggest that cells of the macrophage lineage in the BM of mice synthesize histamine.
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PMID:Histamine synthesis by cells of the macrophage lineage in bone marrow of mice. 754 1

1. Our previous work has shown that injection into mice of lipopolysaccharide (LPS) and the cytokines interleukin 1 (IL-1) and tumour necrosis factor (TNF) induces histidine decarboxylase (HDC), the enzyme forming histamine, in various tissues such as liver, lung, spleen and bone marrow, but not in the blood. The induction of HDC also occurs in nude mice and mast cell-deficient mice. On the other hand, haematopoietic cytokines such as IL-3, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage CSF (GM-CSF) only induce HDC in the haematopoietic organs, i.e. bone marrow and spleen. In the present study, the effect of macrophage depletion on the induction of HDC was examined. 2. On day 1 after a single intravenous injection of a macrophage depletor (liposomes encapsulating dichloromethylene diphosphonate, which is toxic when ingested into macrophages), macrophages were almost completely depleted in the liver and reduced by about 50% in the spleen and bone marrow, but not significantly affected in the lung. On day 3, the degrees of the depletion were similar to those of day 1. In the spleen, macrophages were depleted in the red pulp, and there was a structural destruction. 3. In macrophage-depleted mice, the induction of HDC by LPS, IL-1 alpha or TNF-alpha was not impaired in the liver, and was potentiated in the lung and bone marrow. The induction of HDC was decreased only in the spleen at day 3. 4. HDC was not induced by LPS in the spleen of the adult rat, which is correspondingly inactive in haematopoiesis.5 These results indicate that the major cells in which HDC activity is induced in response to LPS, IL-1 and TNF are not circulating granulocytes, circulating monocytes, T cells derived from thymus, mast cells or phagocytic macrophages. Based on these results, we discuss the possibility that the major cells in which HDC was induced in non-haematopoietic and haematopoietic organs were endothelial cells and haematopoietic precursor cells respectively.
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PMID:Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor. 771 16

To clarify the base of in vivo biological activities of peptidoglycans of Gram-positive bacteria, the effects of a polysaccharide peptide of Staphylococcus epidermidis peptidoglycan (SEPS) on the synthesis of histamine and putrescine in BALB/c mice were examined and compared with those of a lipopolysaccharide (LPS or endotoxin) of Gram-negative bacteria. Within a few hours after its injection into BALB/c mice, SEPS induced histidine decarboxylase (HDC), the enzyme forming histamine, in the liver, lung, spleen and bone marrow, and ornithine decarboxylase (ODC), the enzyme forming putrescine, in the tissues except for the lung. SEPS induced HDC activity even in mast cell-deficient mice and in nude mice. These effects of SEPS were essentially the same as those of LPS. However, the dosage of SEPS capable of inducing HDC and ODC was much higher (100 to 1,000 times) than that of LPS. We have reported that C3H/HeN mice are resistant to SEPS in producing acute arthritis, and their productions of IL-1 and prostaglandin E2 are less than BALB/c mice sensitive to producing acute arthritis. In the present study, it was also found that C3H/HeN mice were markedly resistant to SEPS in inducing HDC activity.
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PMID:Stimulation of the synthesis of histamine and putrescine in mice by a peptidoglycan of gram-positive bacteria. 807 26

The effect of intracerebroventricular (icv) administration of lipopolysaccharide on histidine decarboxylase activity and histamine content in the hypothalamus were investigated in male mice of ddY strain in vivo. Two-fold increase in histidine decarboxylase activity (HDC) was observed 4 h after administration of 50 mcg lipopolysaccharide, and HDC activity returned to the basal level within 12 h after injection. Furthermore, histamine contents showed a slight decrease at 1 and 2 h and a mild increase at 12 h after administration. However, changes in histamine content were not statistically significant. These results suggest that the increase of HDC activity in the hypothalamus by lipopolysaccharide may be involved in the central neuroimmune responses.
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PMID:Increase of histidine decarboxylase activity in mice hypothalamus after intracerebroventricular administration of lipopolysaccharide. 830 15

Promyelocytic HL-60 cells differentiated into mature cells when they were cultured in the presence of dimaprit (10(-4) M), a histamine H2 agonist. An injection of Escherichia coli lipopolysaccharide increased the activity of histidine decarboxylase in bone marrow cells in C3H/HeN mice to a much greater extent than in C3H/HeJ mice, which are resistant to various effects of lipopolysaccharide. Histamine production increased concomitantly. In WBB6/F1 (W/W(v)) mice, which are genetically deficient in mast cells, histidine decarboxylase activity increased more than in C3H/HeN mice. Pure (>99% nonspecific esterase, CD14 and Mac-1 positive) macrophage populations were obtained from long-term culture of the bone marrow cells (bone marrow-derived macrophages, BMDM). Culture of the cells in the presence of lipopolysaccharide caused a slight, but dose-dependent increase in histidine decarboxylase-associated histamine synthesis. Granulocyte/macrophage colony-stimulating factor (rmGM-CSF) or interleukin 3 (rmIL-3) potently increased lipopolysaccharide-induced histamine formation.
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PMID:Role of histamine produced by macrophages in mouse bone marrow. 875 Jul 90


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