Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HISTAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMed1988

Identification of a histamine release inhibitory factor (HRIF) and an inhibitor of histamine releasing factor synthesis (IHS) produced by guinea pig lymphoid cells.

Guinea pig spleen cells, thymocytes, and blood mononuclear cells have been shown to produce a histamine releasing factor (HRF) spontaneously or after stimulation with PHA or specific antigens. In this study we have shown that antigenic stimulation of spleen cells obtained from animals immunized with high doses of antigen suppresses the spontaneous HRF production. Likewise, stimulation with Con A of spleen cells also inhibits the spontaneous HRF production. When the supernatants from Con A- and antigen-stimulated cultures were added to fresh thymocyte cultures, a significant inhibition of HRF production was observed. These supernatants also inhibited HRF-induced histamine release from mast cells. We have identified an inhibitor of HRF synthesis (IHS) and also a histamine release inhibitory factor (HRIF) by gel chromatography. Virtually all mitogen- and antigen-stimulated culture supernatants elaborated the activities of HRF, IHS, and HRIF in various quantities depending on the dose of antigen and the kind of adjuvant used for immunization. IHS has a MW of 22K-35K and 10K. This cytokine also inhibits DNA synthesis by thymocytes. HRIF has a MW of 15K-20K and 10K. It inhibits both HRF- and antigen-induced histamine release from lung mast cells. These results suggest that lymphocytes produce a variety of factors which function to regulate histamine release from mast cells.

Animals↗
PubMed2003

Histamine-immunoreactive neurons of the tuberomammillary nucleus are innervated by alpha-melanocyte stimulating hormone-containing axons. Generation of a new histamine antiserum for ultrastructural studies.

Leptin regulates the release of histamine in the hypothalamus, however, the histaminergic neurons contain few leptin receptors. To reveal that alpha-melanocyte stimulating hormone (alpha-MSH)-containing neurons of the arcuate nucleus may mediate the effects of leptin to the histaminergic neurons, we studied the putative innervation of histamine-immunoreactive (IR) neurons by alpha-MSH-containing axons using double-labeling immunocytochemistry. In order to analyze the relationship of alpha-MSH- and histamine-IR elements, we also generated an antiserum against histamine that is compatible with acrolein-based fixatives commonly used for immuno-electron microscopic studies. The apposition of alpha-MSH-IR axons to histaminergic neurons was observed in all five subnuclei of the tuberomammillary nucleus. Both axo-somatic and axo-dendritic contacts were found. At the ultrastructural level, silver-intensified colloidal gold particles identified the histaminergic neurons, whose ultrastructure was well preserved after fixation with acrolein demonstrating that the new antiserum is a useful tool for the ultrastructural examination of the histaminergic system. The histamine-IR cells received synaptic inputs from alpha-MSH-IR axon terminals visualized by diaminobenzidine. These data indicate that alpha-MSH-synthesizing neurons innervate histaminergic neurons in the tuberomammillary nucleus and may relay the hormonal influence of leptin to the histaminergic system.

Acrolein↗
PubMed1982

[Plasma histamine assay in anaphylactoid reactions of the anesthetized subject. Effects of collection methods and plasma preparation on measured histamine].

Plasma histamine assay in man is indicated for the diagnosis of histamine release, as well as the elucidation of the mechanisms of adverse drug reactions, and the identification of clinical situations in anaesthesia and surgery where a pathological plasma histamine level may occur. Normal and pathological plasma histamine levels vary considerably in the literature. Data from various studies, especially one involving 300 patients in Heidelberg (G.F.R.), allow us to define the normal range for human plasma histamine as 0-1.0 ng . ml-1 . Values greater than 1 ng . ml-1 have to be considered as pathological. The problems related to blood collection and plasma preparation are considered here. Any judgement concerning the method described in the test must take into consideration our long experience of 15 years with it, its reliability in clinical conditions, its practicability, its relatively low cost, and finally, the absence of radioisotopes.

Adult↗
PubMed1981

Histamine production during the anti-allograft response. Demonstration of a new lymphokine enhancing histamine synthesis.

Histamine production is greatly increased during culture of allograft recipient spleen cells in the presence of immunizing cells (secondary mixed leukocyte cultures [MLC]) as compared to that found in primary MLC (i.e., without previous allograft). This phenomenon appears after 24 h of culture and reaches its maximum at 48 h. Optimal increased histamine production is observed when MLC is performed with spleen cells removed from mice during rejection. This increased production of histamine during secondary MLC results from the action of a lymphokine: the histamine-producing cell stimulating factor (HCSF). This factor is released by T lymphocytes. Its production requires specific stimulation of the recipient lymphocytes because increase in histamine production during secondary MLC can be only observed when recipient cells are cultured with stimulating cells bearing at least one homology at K or D loci with immunizing cells. HCSF acts on a cell which is present in bone marrow, spleen, blood, and peritoneal cells but absent in thymus or lymph node cells. This target cell is found in the less-dense layer of a discontinuous Ficoll-gradient of bone marrow cells. HCSF is heat stable, destroyed by trypsin treatment, and has a molecular weight between 50,000 and 100,000. It acts on its target cells by increasing histidine decarboxylase activity.

Animals↗
PubMed1984

Histamine metabolism in patients with histidinemia: determination of urinary levels of histamine, N tau-methylhistamine, imidazole acetic acid, and its conjugate(s).

Histamine metabolism in histidinemic patients was studied by measuring the urinary levels of histamine and its metabolites. The urinary excretions of histamine, N tau-methylhistamine, imidazole acetic acid, and its conjugate(s) were higher in patients with histidinemia than in controls, and these levels of excretion were correlated with the plasma histidine level. The urinary histamine levels of patients with eczema-like dermatitis were twice that of those without dermatitis. The urinary excretion of 3-methylhistidine showed a close correlation with the urinary histidine excretion. Thus, it was concluded that histamine metabolism is higher in histidinemic patients than in normal controls.

Amino Acid Metabolism, Inborn Errors↗
PubMed1994

Histamine production by wine lactic acid bacteria: isolation of a histamine-producing strain of Leuconostoc oenos.

Populations of Leuconostoc oenos were harvested from wines containing a relatively high concentration of biogenic amines. Cultivation of the biomass in synthetic media and wine showed that it consisted of histamine-producing strains. Histamine levels after culture depended on the quantity of precursor available and on the presence of yeast lees, which certainly enriched the medium in histidine. Ethanol and pH, which control bacterial growth rate and total population, were also significant factors: pH and low ethanol concentration enhanced histamine production. Strain Leuc. oenos 9204 was isolated and studied since it retained its ability to produce histamine after several transfers. In synthetic medium this strain produced large amounts of histamine especially in the poorest nutritional conditions (no glucose, no L-malic acid). These results clearly demonstrate that Leuc. oenos involved in wine-making might play a role in biogenic amine production. The vinification method might also influence the final amine concentration in wine.

Biogenic Amines↗
PubMed1987

Inhibition of basophil histamine release by gangliosides. Further studies on the significance of cell membrane sialic acid in the histamine release process.

Histamine release from human basophils was inhibited by preincubation of the cells with a glucolipid mixture containing sialic acid-containing gangliosides. This was true for histamine release induced by anti-IgE, Concanavalin A and the calcium ionophore A23187, whereas the release induced by S. aureus Wood 46 was not affected. It was demonstrated that the inhibitory capacity of the glucolipid mixture could be attributed to the content of gangliosides, since no inhibition was obtained with cerebrosides or with gangliosides from which sialic acid was removed. Preincubation of the cells with the glucolipid mixture increased the sialic acid content of the cells, and this increase was attributed to an insertion of gangliosides into the cell membrane. The inhibition of histamine release was abolished by increasing the calcium concentration, which substantiates our previous findings that cell membrane sialic acid in basophil leukocytes is involved in the regulation of histamine release, possibly by a modulation of the transmembraneous calcium fluxes preceding histamine release.

Basophils↗
PubMed1984

Dural mast cells: source of contaminating histamine in analyses of mouse brain histamine levels.

Histamine levels were determined in mouse brains from WBB6F1-+/+ (mast cell normal) and WBB6F1-W/Wv (mast cell-deficient) mice whose brains were dissected immediately after decapitation or after freezing the severed heads in liquid nitrogen for 10 s. In WBB6F1-+/+ mice, brains obtained from frozen heads contained significantly higher levels of histamine than those obtained from unfrozen heads. The converse was found in brains obtained from the WBB6F1-W/Wv mice. When CF-1 mice (which also contain brain-associated mast cells) were treated as described above, results very similar to those found with the WBB6F1-+/+ mice were obtained. Further, the high levels of histamine found in CF-1 mice whose brains had been frozen in situ were accompanied by an extensive degranulation of mast cells in the dura mater of these mice. Because of this degranulation of mast cells, and the fact that increased levels of brain histamine were not found in mast cell-deficient mice, it is concluded that dural mast cells are the likely source of the artifactually higher levels of histamine seen in brains frozen in situ.

Animals↗
PubMed1982

A simplified method for the extraction and isolation of histamine from whole blood, plasma and tissues for fluorometric histamine analysis.

A simplified method for the extraction and isolation of histamine from blood, plasma and freeze-dried tissue is described. Extraction is carried out with absolute or 80% ethanol. Subsequently histamine is isolated from an ion-exchange column and determined fluorometrically. The normal histamine contents of blood, plasma and various organs from guinea pigs are investigated by this procedure. The values obtained are compared with the data in the literature. On comparison of the histamine contents in the organs of guinea pigs of two weight and age classes, significant differences are found in the lungs, heart, spleen, kidneys and stomach. There seems to be an inverse relationship between body weight and histamine concentration.

Animals↗
PubMed1981

Complement activation requirements for histamine release from human leukocytes: influence of purified C3ahu and C5ahu on histamine release.

The activation of human sera for histamine release by zymosan and anti-BSA-BSA complexes at equivalence was dose dependent and associated with a marked fall in CH50, C3 and C5 hemolytic activities. Heat-aggregated IgG, though able to fix greater than 90% of human CH50 activity and produce a lesser fall in C3 and C5 activities than zymosan and BSA-anti-BSA complexes, was unable to induce basophil histamine release. Chemically purified human C3a and C5a each caused histamine release from human basophils; C5a was more potent than C3a. In addition, neither zymosan nor BSA-anti-BSA complexes released histamine when incubated with homozygous C3-deficient serum. The addition of C3a and C5a at suboptimal concentrations produced an additive effect of histamine release.

Anaphylatoxins↗
PubMed1990

Detection of histamine release inhibitory factor- and histamine releasing factor-like activities in bronchoalveolar lavage fluids.

Histamine releasing factors (HRF) are a group of cytokines that cause degranulation of basophils and mast cells. Recently we have described a histamine release inhibitory factor (HRIF) that inhibits HRF-induced histamine release from basophils and mast cells. The objective of this study was to investigate the presence of these cytokines in bronchoalveolar lavage (BAL) fluid from normal subjects. We found that BAL fluids from 12 to 17 volunteers contained a dialyzable (molecular weight cutoff 3500) factor that inhibited basophil histamine release by HRF, anti-IgE, concanavalin A, and N-formyl-methionyl-leucyl-phenylalanine (FMLP). In addition, BAL fluids from 83% of the tested donors contained a nondialyzable inhibitor that blocked HRF-induced histamine release from basophils. The molecular weight of this inhibitor was estimated to be 20 to 30 and 8 to 10 kD by Sephadex G-50 chromatography and TSK 2000 size-exclusion HPLC. None of the unconcentrated BAL fluids showed any HRF activity on initial screening using basophils from allergic subjects. However, when the BAL fluids were concentrated, all BAL samples that were tested (N = 10) demonstrated significant HRF activity. The molecular weight of BAL HRF has been estimated to be in the range of 15 to 25 kD by size-exclusion HPLC, similar to the HRF synthesized by mononuclear cells. Thus we have demonstrated the presence of both HRF and HRIF in the BAL fluids. We speculate that these cytokines may be involved in the local regulation of basophil and mast cell activation.

Adult↗
PubMed1992

The stimuli releasing histamine from murine bone marrow-derived mast cells (BMMC). 3. Effect of coculture with 3T3 fibroblasts on the histamine releasability of BMMC.

Murine bone marrow-derived mast cells at 3 wk in culture were further cultured in the absence (N-BMMC) or presence (F-BMMC) of 3T3 fibroblasts in the medium containing LI-3, and were examined for their functional responses to either histamine releasing stimuli such as compound 48/80 or an inhibitor of histamine release, disodium cromoglycate. After 3 weeks in coculture with 3T3 fibroblasts, the mast cells increased their histamine content greater than 10 fold, and greater than 10% of the cells changed histochemically to become safranin positive. F-BMMC released approximately 10% histamine when challenged with compound 48/80 or substance P, whereas N-BMMC failed to do so. Furthermore, when the sensitized cells were challenged with DNP-HSA antigen, histamine release from F-BMMC but not from N-BMMC was inhibited by preincubation with disodium cromoglycate. We also examined changes in intracellular Ca2+ ([Ca2+]i) in the cells when challenged with compound 48/80. A transient increase in [Ca2+]i was observed on stimulation with the compound in F-BMMC but not in N-BMMC. Taken together, our results indicate that the interleukin 3-dependent cultured murine mast cells change functionally, as well as histochemically, into in vitro counterparts of connective tissue mast cells when cocultured with 3T3 fibroblasts and may be useful tools for analyzing the mechanisms involved in degranulation from connective tissue-type mast cells.

Animals↗
PubMed1985

Histamine release by esterase inhibitors. The regulation of histamine release from human leukocytes of allergic and non-allergic individuals by the serine esterase inhibitors diisopropyl fluorophosphate and pinacolyl methylphosphorofluoridate.

The serine esterase inhibitor diisopropyl fluorophosphate (DFP) has been shown to inhibit IgE-dependent histamine release. Recently, it has been demonstrated that lower concentrations of DFP enhanced IgE-dependent histamine release and inhibited desensitization. This manuscript describes the ability of another esterase inhibitor, pinacolyl methylphosphorofluoridate (soman), to directly cause release of histamine from human leukocytes (basophils) by a process that is IgE-independent. This release process requires calcium and is also temperature-dependent but occurs over a longer period of time than IgE-dependent release. These data suggest that there is a serine esterase which controls histamine release, and inhibition of this esterase causes histamine release.

Enzyme Inhibitors↗
PubMed1986

[Histamine receptor-bearing lymphocytes. VII. Antibody formation and graft-vs-host reaction from spleen cells after separation on histamine affinity columns].

Histamine-ovalbumin conjugates were characterized in respect to the relative amount of histamine residues which are accessible to membrane receptors. These conjugates were bound to a protein carrier. Spleen cells exhibited an enhanced reactivity in the adoptive antibody production as well as the graft versus host reaction after filtration through affinity columns with a low density of histamine residues. Contrary to that, the use of affinity columns with high histamine density led to a reduced immunoreactivity of the nonadherent cells. Consequently, controversial literature data concerning this problem seem to be based on methodological differences. The results support the hypothesis, that suppressor cells carry more histamine receptors than other immunoreactive cells.

Animals↗
PubMed1988

[Comparative study of 3 positive controls for routine prick tests in children: 48/80, 1 mg histamine and 5 mg histamine].

We compared, among 153 children 2 to 14 years old, responses to some positive control solutions for prick tests made with a Stallerpoint. We obtained the following values: -6% - 48/80:4.46 +/- 1.88 mm -1 mg/ml Histamine:3.49 +/- 1.67 mm -5 mg/ml Histamine:5.13 +/- 1.78 mm. 1 mg/ml histamine gives too many null responses (12/153) to represent a valuable positive control. 5 mg/ml histamine, on the other hand, gives some very strong reactions which may induce an underestimation of responses to allergen tests. Compound 48/80 seems to remain the best positive control for prick test exploration of immediate allergy in children. An alternative might be an intermediate solution of histamine 2.5 mg/ml.

Adolescent↗
PubMed1979

[The secretory action of various C-5-alkylsubstituted histamines and N alpha-methyl-histamines on anaesthetized cats with Heidenhain pouches (author's transl)].

In particular, the action of N alpha-methyl-histamine has to be considered since its secretory response is approximately 1.5 times greater than that of histamine and its secretion lasted for a longer period of time. After C-5-alkylsubstitution, both 5-methyl-histamine and N alpha,5-dimethyl-histamine showed secretory action comparable to that of histamine; the agonistic activity, however, decreased with increasing chain length.

Animals↗
PubMed1983

Skin allografts generate an enhanced production of histamine and histamine-producing cell-stimulating factor (HCSF) by spleen cells in response to T cell mitogens.

In response to T cell mitogens, spleen cells produce a large amount of histamine, whereas no or a slight increase is observed after B cell mitogen stimulation. This increased histamine production results from the effect of a factor having all the characteristics of HCSF (histamine-producing cell-stimulating factor) already described in secondary MLC supernatant. This factor is produced by Thy-1, 2, Lyt-1, 2-positive cells. Spleen cell cultures derived from skin-allografted mice during rejection produce more histamine in response to T cell mitogens than do spleen cells from normal or syngeneic grafted mice. Such a phenomenon is not observed in response to B cell mitogens. A striking association is found between enhanced histamine synthesis and skin allograft rejection. This phenomenon results from a) a five to 10-fold increase in HCSF production by allograft recipient spleen cells in response to T cell mitogens, and b) an increase in HCSF sensitivity of these spleen cells.

Animals↗
PubMed1982

Interaction of histamine with adrenergic smooth-muscle neurotransmission. II. Significance of calcium ions for the effects of histamine on contractions induced by endogenous noradrenaline.

The role of Ca2+ for the effects of histamine on contractions induced by electrostimulation has been studied on smooth-muscle organs with adrenergic neurotransmission (rat anococcygeal muscle and vas deferens). The low Ca2+-concentrations in the organ bath (below 1.8 mM) reduce the amplitude of the smooth-muscle contractions in response to electrostimulation (more markedly at the low frequency), at the same time potentiating the inhibitory action of histamine on the electrostimulation-induced contractions of the isolated preparations. Raising the Ca2+-concentration in the nutrient medium increases the magnitude of the contractions in response to electrostimulation. At the same time the high Ca2+-concentrations weaken the second (inhibitory) phase of the action of histamine on the electrostimulation-induced contractions of the smooth-muscle preparations. The potentiating action of histamine on contractions in response to electrostimulation is not essentially influenced by the changes in Ca2+-concentration. The data obtained show that Ca-ions may play a role in the mechanism of the inhibitory action of histamine on the smooth-muscle adrenergic neurotransmission, which is assumed to be mediated by presynaptic H2-histaminergic receptors.

Animals↗