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At least 1,261 records · Page 70Linked to original sources
PubMed1986

Forskolin inhibits the release of histamine from human basophils and mast cells.

We found that forskolin (10(-7) to 3 X 10(-5) M) caused dose-related inhibition of antigen-induced histamine release from human basophil leukocytes. The dose-response inhibition curve was paralleled by a forskolin-induced increase in cyclic AMP (cAMP) levels in human leukocyte preparations. The kinetics of inhibition of histamine release and of the increase in leukocyte cAMP were the same. In a second series of experiments we evaluated the effect of forskolin on antigen-induced histamine release from chopped human lung passively sensitized with serum from an allergic patient. Forskolin (10(-7) to 3 X 10(-5) M) dose-dependently inhibited the release of histamine from human lung mast cells. Thus forskolin appears to modulate the release of mediators of the immediate hypersensitivity reaction, presumably through activation of adenylate cyclase in human basophils and mast cells.

Adult↗
PubMed1986

Immunologic histamine release from isolated human basophils during specific immunotherapy.

Anti-IgE- and antigen-induced histamine release from basophils isolated from 20 atopic patients sensitive to grass pollen allergens was evaluated. The studies were made before and after short-term immunotherapy with Pollinex. It was shown, that after hyposensitization a significant decrease on anti-IgE and specific antigen-induced histamine release from basophils occurs.

Allergens↗
PubMed1981

Antigen-induced histamine release from mast cells and basophils after hydrocortisone and disodium cromoglycate treatment.

The effect of drugs applied in the treatment of allergic diseases such as hydrocortisone and disodium cromoglycate-Intal on the release of histamine during immediate allergic response was investigated. Experiments carried out on guinea-pigs showed that after hydrocortisone administration the blood histamine level fell, whereas the histamine concentration in the lung tissue varied, depending on the time of the drug administration in relation to the antigen challenge. Disodium cromoglycate give before induction of an asthma attack in guinea-pigs lowered the histamine level in the blood and in the lung tissue homogenates. Investigations were also carried out on isolated rat mast cells and human basophils. The stabilizing effect of hydrocortisone was much weaker than that of disodium cromoglycate especially regarding mastocytes. It was found that the extent of histamine release from mastocytes and basophils depends on the concentration of the drugs applied and on the type of antigen used for induction of cell degranulation.

Allergens↗
PubMed1987

Membrane sialic acid influences basophil histamine release by interfering with calcium dependence.

The influence of the cell membrane content of sialic acid on basophil histamine release was examined in vitro in allergic patients and normal controls. Enzymatical removal of sialic acid enhanced histamine release induced by allergen and anti-IgE, whereas an increase in membrane sialic acid content by insertion of sialic acid containing gangliosides into the membrane inhibited the mediator release. The reduction in membrane sialic acid content abolished the inhibitory capacity of the calcium channel antagonist nimodipine, whereas the inhibition produced by verapamil and lanthanum was not affected. This difference, together with the previous finding that alterations in membrane sialic acid content is reflected in the cell sensitivity to extracellular calcium, suggest an interaction between membrane sialic acid and the calcium channels involved in basophil histamine release.

Basophils↗
PubMed1988

Virus enhances histamine release from human basophils.

Histamine release from human basophil leukocytes was triggered by Staph. aureus or by complement activation caused by endotoxins isolated from E. coli or Salmonella bacteria. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus itself did not release histamine. The potentiating effect of the virus was abolished by a potent neuraminidase inhibitor. Furthermore, a purified neuraminidase preparation obtained from Vibrio cholerae caused a similar potentiating effect, which was also abolished by the neuraminidase inhibitor. These findings indicate that the neuraminidase on the surface of influenza A virus is responsible for the potentiating effect of the virus on basophil histamine release.

Basophils↗
PubMed1988

Inhibition of basophil histamine release by methotrexate.

Basophil leukocytes in whole blood from 4 healthy donors, 4 atopic patients, and 10 female patients operated for breast-cancer were preincubated from 1 to 20 hrs alone or in the presence of methotrexate (MTX) or MTX and folinic acid. After preincubation, the basophil leukocytes were challenged with anti-IgE, allergens or the calcium ionophore A23187 in the presence of 25 ng/ml TPA (12-o-tetradecanoyl-phorbol-13-acetate). A 9-hr preincubation with MTX produced significant inhibition of histamine release (greater than 20%) at 500-50 micrograms/ml. This effect increased up to 20 hrs of incubation, displaying maximal activity (100% inhibition) at 500 micrograms/ml, but even submicrogram concentrations (0.5 microgram/ml) produced significant inhibition. The addition of folinic acid did not alter the inhibition. It is concluded that MTX with or without the addition of folinic acid is a potent inhibitor of histamine release induced by anti-IgE, allergens, and A23187 combined with TPA. Like glucocorticoids the mechanism of action of MTX may be linked to arachidonate metabolism, but may interrupt earlier steps in prostaglandin synthesis.

Adult↗
PubMed1988

Basophil histamine release studies in the evaluation of a new anaesthetic agent.

Propofol (2,6-diisopropylphenol) has recently been introduced into clinical practice as an induction agent. This study evaluated the effect of propofol on basophil histamine release in 13 healthy subjects. No release was demonstrated in 11 subjects. Two subjects released histamine at the highest drug concentration, one also releasing at lower concentrations. Both subjects whose basophils released histamine in response to propofol were anaesthetists using the drug during the course of their practice.

Anesthetics↗
PubMed1983

Basophils in human disease.

Hypersensitivity reactions containing significant infiltrates of basophils occur in a large proportion of allergic diseases such as contact dermatitis, atopic dermatitis, and allergic rhinitis, and are quite deleterious. However, the potential usefulness of such responses can be recognized in similar reactions in guinea pigs responding to tissue invasion by complex multicellular parasites in which interactions occur between thymic-derived T lymphocytes, antibodies, and basophils in immune resistance responses. Perhaps inappropriate and deleterious allergic responses to pollens, chemicals, and insects is the price that we must pay for the ability to reject complex parasites.

Animals↗
PubMed1997

The effect of recombinant stem cell factor on human skin and lung mast cells and basophil leukocytes.

Recombinant human stem cell factor (rhSCF) induced histamine release from human skin and lung mast cells but had no effect on human basophil leukocytes. More importantly, rhSCF enhanced the release of histamine in response to IgE-crosslinking of human mast cells. This potentiation was observed at rhSCF concentrations which induced histamine release, and also at lower concentrations of the ligand which by themselves produced no effect. Very limited potentiation was observed with human basophil leukocytes. The enhancing effect of SCF was unique to IgE-dependent stimulation and when SCF was incubated with the neurotransmitter substance P and the calcium ionophore A23187, no augmentation of histamine release was observed with any of the cell types tested. These findings suggest that endogenous SCF may contribute to the regulation of mast cell function and may hence play a role in diverse allergic and inflammatory reactions.

Antibodies, Anti-Idiotypic↗
PubMed2001

Serum IgE specific to indoor moulds, measured by basophil histamine release, is associated with building-related symptoms in damp buildings.

OBJECTIVE: To study the relationship between basophil histamine release (HRT) to indoor moulds, indicating specific IgE, and building-related symptoms (BRS), asthma, and hay fever in individuals working in damp and mouldy buildings. METHODS: A cross-sectional study was performed among 86 school staff members, who on average had worked 143 months (range: 3-396) in moist buildings with mould growth in the constructions. A questionnaire concerning mucous membrane symptoms, facial skin symptoms, central nervous system symptoms, hay fever, and asthma was fulfilled by the participants, and blood samples were taken. Eight mould species growing on building constructions were identified and cultivated to obtain allergenic materials for testing. The presence in serum of IgE specific to moulds was verified by histamine release test (HRT) based on passive sensitization of basophil leukocytes. The validity of the method was confirmed by parallel testing of patients allergic to grass- and birch pollen and by the shift from positive to negative response after removal of serum IgE and by using sham sensitization. RESULTS: The prevalence of most BRS was between 32% and 62%. Positive HRT, showing serum IgE specific to one or more of the moulds, was observed in 37% of the individuals. The highest frequency of positive HRT was found to Penicillium chrysogenum and then to Aspergillus species, Cladosporium sphaerospermum and Stachybotrys chartarum. A significant association was found between most BRS and positive HRT, whereas no association was observed between positive HRT to moulds and self reported hay fever or asthma. CONCLUSION: Positive HRT to indoor moulds, showing the presence in serum of IgE specific to the fungi, was found to be related to BRS in individuals working in damp and mouldy buildings. Whether the association is of causal character is a question for further studies. The test may be useful in the evaluation and study of possible mould induced BRS.

Adult↗
PubMed2001

Differential response of mast cells separated from various organs and basophils of dogs to the fluoroquinolone antimicrobial levofloxacin.

Histamine releases induced by the fluoroquinolone antimicrobial levofloxacin (LVFX) were investigated using mast cells separated from various organs and peripheral basophils of dogs, being the most susceptible species to quinolone derivatives, in both in vivo and in vitro systems. An intravenous infusion of LVFX at 30 mg/kg over a 30-min period produced endogenous histamine release from 5 min, and a maximum at 30 min, in which the plasma LVFX concentration was approximately 50 microM. A close correlation (r = 0.87, n = 20) between histamine and LVFX concentrations in plasma during the infusion was observed. In the in vitro study, LVFX at 30 microM or more caused histamine release from mast cells separated from the liver and skin, but not from the gastric mucosa, lung, and peripheral basophils. More exactly, the liver mast cells were most susceptible to LVFX among the organs tested. On the other hand, compound 48/80, a prototype histamine liberator, elicited the histamine release from the liver or skin mast cells at 10 microg/ml, and the calcium ionophore A23187 at 1 microM exhibited the histamine release from the mast cells derived from all organs examined. Histochemical analysis revealed that the liver and skin mast cells had positive reaction for both alcian blue and safranin staining, but the gastric mucosa and lung mast cells were only positive for alcian blue staining, indicating that LVFX preferably activated the connective tissue-type mast cells rather than the mucosal-type mast cells. The degranulation of the liver and skin mast cells brought about by either LVFX or compound 48/80, unlike the calcium ionophore A23187, was blocked by pretreatment with pertussis toxin, suggesting the involvement of pertussis toxin-sensitive G proteins. The results obtained from the canine experiments strongly suggest that LVFX induces histamine release from the connective tissue-type mast cells distributed mainly in the liver, somewhat in the cutaneous tissue, through the activation of pertussis toxin-sensitive G proteins.

Animals↗
PubMed1984

Solubilization and characterization of the leukotriene C4 synthetase of rat basophil leukemia cells: a novel, particulate glutathione S-transferase.

Rat basophil leukemia cell homogenates effectively catalyze the conversion of leukotriene A4 to a mixture of leukotrienes C4 and D4 in the presence of glutathione. These homogenates also catalyze the formation of adducts of halogenated nitrobenzene with glutathione, as determined spectrophotometrically. While all the classical glutathione S-transferase activity resides in the soluble fraction of the homogenates, the thiol ether leukotriene-generating activity is found in the particulate fraction. This "leukotriene C synthetase" activity has been solubilized from a crude high-speed particulate fraction by means of the nonionic detergent, Triton X-100. The solubilized enzyme is incapable of converting 2,4-dinitrochlorobenzene to a colored product in the presence of glutathione. Nor will it react with 3,4-dichloronitrobenzene. On the other hand, under optimal conditions, this enzyme preparation is capable of generating about 0.1 nmol leukotriene C mg protein-1 min-1 in a reaction which continues in linear fashion for at least 10 min. This dissociation in substrate specificity, as well as differences in the inhibition profile, distinguish the enzyme activity in the particulate fraction from rat basophil leukemia cell homogenates from the microsomal glutathione S-transferase which has been described in rat liver homogenates, suggesting that this "leukotriene C synthetase" is a new and unique enzyme.

Animals↗
PubMed1989

Modulation by phorbol 12-myristate 13-acetate of arachidonic acid release from rat basophilic leukemia cells stimulated with A23187.

Rat basophilic leukemia (RBL-2H3) cells were cultured in medium containing [3H]arachidonic acid and labelling of the different lipid fractions was followed with time. After up to 4 h of culture, the label was found mostly in phosphatidylcholine. After 8 h, labelling of phosphatidylethanolamine gradually exceeded that of phosphatidylcholine, until at 24 h, approximate equilibrium labelling of the lipid fractions was attained and 45% of the label was found in phosphatidylethanolamine, 35% in phosphatidylcholine, 18% in the phosphatidylserine/inositide fraction and the remainder in the neutral lipid fraction. Stimulation of cells with A23187 after 30 min of labelling caused release of [3H]arachidonic acid which was accountable by a decrease in radioactivity of phosphatidylcholine, whereas stimulation of cells after 24 h of labelling caused the release of radioactive arachidonic acid, which was accompanied by a decrease of label in both phosphatidylcholine and phosphatidylethanolamine. Incubation of the labelled cells with phorbol 12-myristate 13-acetate prior to ionophore addition enhanced both the release of [3H]arachidonic acid and its metabolites and the decrease in label of the same phospholipids as those affected by ionophore alone. Under our conditions, the enhancement effects of phorbol ester were greatest after 2-5 min of preincubation, prior to ionophore addition. The results suggest that in basophilic leukemia cells, arachidonic acid release proceeds from several pools of phospholipids and that the activity of the phospholipase(s) involved is modulated by protein kinase C.

Animals↗
PubMed1983

RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and related compounds. Novel inhibitors of histamine release from rat mast cells and human basophils.

RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and twenty-five related 5-substituted oxadiazolones have been investigated for their antiallergic activities in three in vitro models of anaphylaxis. Sixteen compounds were potent (I50 less than or equal to 50 microM) inhibitors of antigen-induced release of histamine (AIR) from rat mast cells (RMC), and seven compounds inhibited anti-IgE-induced release of histamine from human basophils (I50 less than or equal to 100 microM). The antiallergic activity profiles of RHC 3288 and three other compounds in these models have been compared with that of disodium cromoglycate (DSCG). As inhibitors of AIR from RMC, RHC 3288, 3334, 3354 and 3380 were 3 to 10 times more potent than DSCG. In the same model (AIR from RMC), activity profiles of all four RHC compounds were identical to that of DSCG in the following respects: loss of inhibitory activity with increasing preincubation time, tachyphylaxis and cross-tachyphylaxis to each other, and inability to inhibit histamine release stimulated by Ca2+ ionophore, dextran + phosphatidyl serine and compound 48/80. RHC 3288, 3334, 3354 and DSCG had no effect in the other two models, histamine release from guinea pig lung mediated predominantly by IgG1 class of antibodies and anti-IgE-induced histamine release from human basophils. We conclude that RHC 3288 is a potent inhibitor of mediator release with a mechanism of action similar to that of DSCG.

Animals↗
PubMed1986

Inhibition of immunological and nonimmunological histamine release from human basophils by adenosine analogues that act at P-sites.

2',5'-Dideoxyadenoside (DDA) inhibited both anti-IgE and ionophore A23187 induced histamine secretion from human basophils. Whereas DDA inhibited IgE-dependent histamine secretion when added at all times prior to challenge, release induced by A23187 was inhibited only with simultaneous addition of DDA and secretagogue. Dipyridamole, but not theophylline, abrogated DDA mediated inhibition of histamine release suggesting an intracellular mechanism of action of DDA. The observations that 2'-deoxyadenosine and 9-beta-D-arabinofuranosyladenine also inhibited release suggest that the its inhibitory effect was enhanced by manganese and reversed by islet activating protein from Bordetella pertussis suggest that DDA inhibits basophil histamine release by interacting with a guanine nucleotide binding protein which may be linked to either adenylate cyclase or other second messenger system(s).

Adenosine↗
PubMed1987

Inhibition of IgE-mediated release of histamine and peptide leukotriene from human basophils and mast cells by forskolin.

Forskolin, a diterpene compound isolated from the roots of Coleus forskohlii, activates adenylate cyclase in membranes from a variety of mammalian tissues. We found that forskolin (10(-7) to 3 X 10(-5) M) caused a concentration-related inhibition of IgE-mediated release of histamine and peptide leukotriene C4 (LTC4) from human basophils and lung mast cells. There was a significant linear correlation between the per cent inhibition of histamine and LTC4 release from both cell types. However, in both systems forskolin exerted a significantly greater inhibitory effect on LTC4 release than on histamine release. The concentration-response inhibition curve was paralleled by a forskolin-induced rise in cAMP levels in human leukocyte and mast cell preparations. The relationship between the effect of forskolin and the cAMP concentration was supported by the finding that forskolin inhibited the "first stage" of antigen-induced histamine release, but not the release caused by the Ca2+ ionophore, A23187. Propranolol, a competitive beta-receptor antagonist, did not block the inhibition of mediator release or the cAMP accumulation caused by forskolin. These data suggest that forskolin modulates the release of mediators of immediate hypersensitivity reactions via the activation of adenylate cyclase in human basophils and mast cells.

Adenylyl Cyclases↗
PubMed1989

Heterogeneity of human mast cells and basophils. Effects of a putative 5-lipoxygenase inhibitor.

The effects of a putatively specific 5-lipoxygenase inhibitor, 2(12-hydroxydodeca-5,10-dinyl)-3,5,6-trimethyl-1,4-benzoquin one (AA-861), and its major metabolite, M-I, were assessed using anti-IgE activated human basophils, lung mast cells and skin mast cells. In basophils and lung mast cells, no effects on histamine release were observed, whereas leukotriene C4 (LTC4) production was inhibited (IC50 values less than 1 microM). In addition, prostaglandin D2 (PGD2) production was inhibited in lung mast cells (IC50 congruent to 5 microM). In contrast, in skin mast cells both histamine release and PGD2 production were reduced by AA-861 and M-I, with IC50 values of congruent to 5 and 0.4 microM for histamine and PGD2, respectively. These data reveal biochemical heterogeneity among human histamine-containing cells and underscore the necessity of assessing a pharmacologic agonist in relevant cell systems.

Arachidonate 5-Lipoxygenase↗
PubMed1990

Modulation of mediator release from human basophils and pulmonary mast cells and macrophages by auranofin.

Auranofin, a new orally absorbable gold compound, inhibits IgE-(anti-IgE) and non-IgE-mediated (f-met-peptide and the Ca2+ ionophore A23187) histamine release from human basophils. Auranofin inhibits the release of histamine induced by phorbol myristate (TPA) and bryostatin 1 both in the presence and absence of extracellular Ca2+. Increasing the Ca2+ concentrations in the extracellular medium does not reduce the inhibitory effect of auranofin on anti-IgE- or A23187-induced secretion. Auranofin inhibits the de novo synthesis of sulfidopeptide leukotriene C4 (LTC4) induced by anti-IgE from basophils and mast cells purified from human lung. However, in both systems auranofin has a significantly greater inhibitory effect on LTC4 release than on histamine secretion. Finally, auranofin induces a concentration-dependent inhibition of A23187-induced leukotrine B4 (LTB4) release from purified human lung macrophages. These data suggest that auranofin modulates the release of preformed (histamine) and de novo synthesized (LTC4 and LTB4) chemical mediators from human inflammatory cells isolated from peripheral blood and human lung tissues.

Auranofin↗