Anaphylactic Histamine Release Research Articles

A modulation of the anaphylactic basophil histamine release by selective H2 histamine agonists.

Two selective H2-histamine agonists, dimaprit and impromidine, have been tested for their action on histamine release from human basophils and rat mast cells. IgE-mediated basophil histamine release was inhibited by stimulation of histamine H2-receptors. However, differences between the actions of both dimaprit and impromidine were noticed. Both impromidine and dimaprit had no specific effect on 48/80-induced histamine release from rat mast cells, although the latter in higher concentrations either slightly increased spontaneous histamine release or non-specifically inhibited compound 48/80-induced release. The results are consistent with the view that activation of adenylate cyclase via H2-histamine receptors might be an important regulatory mechanism of histamine release from human basophils but not from rat mast cells.

Are the anti-allergic actions of theophylline due to antagonism at the adenosine receptor.

Adenosine potentiated anaphylactic histamine release from isolated rat mast cells in a dose-dependent manner between 10(-8) and 10(-5) M. Adenosine was found to be present during a normal incubation of mast cells, but the concentration was low (2 x 10(-8) M). In rat plasma the concentration was 1.5 x 10(-7) M. The effect of 10(-5) M adenosine was dose-dependently inhibited by theophylline. 50% inhibition was found at 3 x 10(-5) M theophylline. Cyclic nucleotide phosphodiesterase inhibition required much higher concentrations (IC50 approximately 10(-3) M). It is suggested that some of the anti-allergic actions of theophylline (clinical concentration range: 10(-5) M) does not involve cyclic nucleotides but may be due to inhibition of the effects of endogenous adenosine.

Characterization of the receptor mediating the antianaphylactic effects of beta-adrenoceptor agonists in human lung tissue in vitro.

1 The rank order of potency of six beta-adrenoceptor agonists as inhibitors of the anaphylactic release of histamine from fragments of passively sensitized human lung in vitro was (--)-isoprenaline greater than (--) -adrenaline greater than (+/-)-salbutamol greater than (--)-noradrenaline greater than R0363 greater than H133/22. 2 The beta-adrenoceptor antagonists, propranolol, atenolol and H35/25, blocked the response to both (--)-isoprenaline and (+/-)-salbutamol competitively. Each antagonist gave similar pA2 values with both agonists. pA2 values were consistently at the high end of the range expected for interaction at a beta 2-adrenoceptor. 3 Practolol did not antagonize isoprenaline in a competitive manner but was a competitive antagonist of salbutamol with a pA2 at the high end of the range expected for interaction at a beta 2-adrenoceptor. 4 Data obtained with agonists are consistent with the receptor being of the beta 2-subtype. Data obtained with antagonists indicate a consistently higher affinity for the receptor than observed for the beta 2-subtype in other tissues but do not suggest a novel beta-adrenoceptor subtype on the mast cell of the human lung.

Effect of prostaglandins on anaphylactic release of histamine and slow reacting substance of anaphylaxis (SR -A) from guinea pig lung tissues (author's transl)

Effect of prostaglandins on anaphylactic release of histamine and slow reacting substance of anaphylaxis (SR -A) from guinea pig lung tissues (author's transl)

Allergen-mediated histamine release from whole blood. Clinical evaluation.

An automated spectrofluorometric histamine assay has been applied to the study of allergen-mediated histamine release on small samples of blood. Histamine released into the plasma following incubation of blood with grass pollen, house dust or cat dander was compared in 35 nonallergic controls and 43 atopic patients sensitive to these allergens by history, skin tests and a high RAST score. 14 of the patients suffering from hay fever were examined after completion of at least 1 year of preseasonal immunotherapy. No allergen-mediated histamine release was observed in most nonallergic controls; a negligible release (< 5% of total blood histamine) was seen in about 10% of these subjects. In contrast, a significant histamine release, ranging from 6 to 48% of total blood content, was specifically induced by allergen in over 90% of patients sensitive to it. Negative results are found more frequently in atopic patients submitted to immunotherapy. In some patients, allergen-mediated histamine release on whole blood was compared to that obtained with the corresponding isolated leukocytes. As expected, a good correlation was found between both systems but anaphylactic histamine release occurs much more quickly in the blood than in the leukocyte suspension. This procedure for measuring histamine released by antigen on blood is easy to perform. Heparinized blood may be stored 48 h without modification in the anaphylactic release of histamine and eight different allergens may be tested with 10 ml of blood. It thus appears to be a useful method for exploring reaginic hypersensitivity and may function as an <i>in vitro</i> alternative to skin tests.

S IV-2 - (Supplement, a) Differential effects of inhibitors of calcium influx on heterologous anaphylactic histamine release from rat mast cells.

S IV-2 - (Supplement, a) Differential effects of inhibitors of calcium influx on heterologous anaphylactic histamine release from rat mast cells.

Histamine-containing cells from bronchial lavage of macaque monkeys. Time course and inhibition of anaphylactic histamine release.

Bronchial lavage of rhesus and cynomolgus monkeys provided leucocyte suspensions with viable histamine-containing cells (HCC) as 1--8% of the white cell population. These HCC released histamine or challenge with antiserum to human IgE. HCC from 2 monkeys with pulmonary and cutaneous hypersensitivity to Ascaris antigen (AA) released histamine on challenge with AA. The extent of histamine release was related to the concentration of antigen and antiserum, and histamine release was complete within 10 min of challenge. (+/-)Salbutamol and (-)isoprenaline were potent inhibitors of anaphylactic histamine release from HCC, but disodium cromoglycate and AH 9679 were relatively poor inhibitors. The HCC system combines the reproducibility of a cell suspension with a response to drugs similar to that of human lung fragments.

Relationship between serum IgE levels and anaphylactic histamine release from isolated rat mast cells.

Inbred Hooded Lister rats were immunized with egg albumin with B. pertussis vaccine used as an adjuvant. The serum levels of total IgE and IgE antibody (egg albumin specific) were determined by radioimmunoassay techniques before and after immunization. The basic level of total IgE in serum was 560 +/- 110 ng/ml. After immunization a maximal peak at day 11 of 1940 +/- 160 ng/ml was registered. Anti-egg albumin IgE antibody showed a maximum around day 13 of 75 +/- 11 units/ml. Pleural mast cells were isolated on Ficoll between day 14 and 20 after immunization. A significant negative correlation between the basic total IgE level and histamine release by antigen (egg albumin) was found and also a significant positive correlation of specific IgE antibody (determined at day 11) and histamine release. The correlation between IgE level and histamine release was slightly improved if instead the ratio of specific IgE antibody over total IgE was used.

Adenosine triphosphate levels during anaphylactic histamine release in rat mast cells in vitro. Effects of glycolytic and respiratory inhibitors

The adenosine triphosphate (ATP) content of rat mast cells was studied during and after anaphylactic histamine release. The almost identical time course of ATP decrease from mast cells treated with either glycolytic or respiratory inhibitors supports the view that the ATP depletion was largely related to the histamine release process and not to an uncoupling of oxidative phosphorylation by an increased concentration of cytosol Ca 2+. The ATP content of the cells was not restored within the 2 h of observation. No inhibition of lactate production from mast cells exposed to antigen in the presence of respiratory inhibitors and glucose was observed. Based on the lactate production from mast cells, the turnover time of ATP was calculated to be about 3 4 min .

Inhibition of anaphylactic histamine release by complexes of lidocaine with zinc

Inhibition of anaphylactic histamine release by complexes of lidocaine with zinc

The 'calcium gating mechanism' in the anaphylactic histamine release from guinea pig mast cells [proceedings

Our results lend support to the validity of the ‘calcium gating hypothesis’ [2] also for the histamine release from guinea pig mast cells.

Diisopropylfluorophosphate-evoked inhibition of anaphylactic histamine release from human skin: decrease of the inhibition by storing the skin specimens

Antigen-induced histamine release from human skin slices passively sensitized with reaginic serum in vitro was inhibited by DFP, suggesting involvement of serine esterase activation in the reaction. The magnitude of DFP-evoked inhibition of the histamine release was not the same in each skin sample and no correlationship was observed between the magnitude of the DFP-evoked inhibition of the histamine release and that of the histamine release in the absence of DFP. The magnitude of the histamine release in the presence of DFP was smaller in the fresh skin than in the stored skin, whereas that in the absence of DFP was greater in the former than in the latter. The inhibitory effect of cytochalasin B on the anaphylactic histamine release from fresh and stored human skin was the reverse of the effect of DFP. The present results indicate that the magnitude of anaphylactic histamine release from human skin does not match that of the activation of serine esterase in the reaction, suggesting the possibility that there may be some factor modulating the activation of serine esterase in the anaphylactic reaction in human skin.

Anaphylaxis in guinea-pig peripheral airways in vitro

The contributions made by histamine, prostaglandins (PG) and slow reacting substances (SRS-A) to anaphylactic contractions in isolated guinea-pig lung were investigated. Histamine, PGF 2α and SRS-A induced isometric contractions in lung parenchymal strips and in tracheal smooth muscle. The effective concentrations of the autacoids were the same in lung strips and tracheas. Anaphylactic contractions in lung strips from bovine serum albumin sensitised animals were not affected by mepyramine (5 × 10 −6 M), or indomethacin (3 × 10 −5 M) but were markedly reduced by FPL 55712 (5 × 10 −5 M) suggesting that SRS-A plays a major role in the anaphylactic response. The effect of isoprenaline on anaphylactic histamine release and contractions was also examined. Anaphylactic contractions in lung strips were inhibited by isoprenaline (10 −10 – 10 −7 M). Isoprenaline also inhibited anaphylactic histamine release from lung parenchyma. 10 −7 M isoprenaline inhibited contractions by 85.6% and reduced histamine release by 27.9%. The results suggest that histmaine release does not contribute markedly to anaphylaxis in peripheral airways.

Anaphylactic release of histamine and slow reacting substance of anaphylaxis (SRS-A) from guinea-pig lung and its modulation by prostaglandins

Anaphylactic release of histamine and slow reacting substance of anaphylaxis (SRS-A) from guinea-pig lung and its modulation by prostaglandins

Antiallergic effects of the adrenergic beta-stimulant trimetoquinol in rats and guinea pigs.

Trimetoquinol (TMQ), like isoproterenol (Iso), inhibited not only the in vitro anaphylactic release of histamine from minced guinea pig lung tissue but also passive cutaneous anaphylaxis (PCA) in rats and guinea pigs and systemic anaphylaxis in guinea pigs. In these inhibitory effects, TMQ was more potent than Iso and other β-adrenergic stimulants (orciprenaline, salbutamol and terbutaline) in vivo, and 1000 times more active than disodium cromoglycate in vitro. In rat PCA, orally administered TMQ was fully effective as early as 5 min after administration and showed a longer duration of action than Iso. Furthermore, TMQ did not greatly affect the vascular permeability, unlike Iso, which markedly inhibited histamine-induced dye leakage on the rat skin, suggesting that the inhibition of PCA by Iso may be partly ascribed to this action on the capillary vessels, and therefore that the anti-anaphylactic activity of TMQ should be that much greater than that of Iso. When rat mast cells were incubated with TMQ, the cellular level of adenosine-3', 5'-cyclic monophosphate (cAMP) was elevated. The inhibition of in vitro histamine release by TMQ and the elevation of cAMP in the mast cells by TMQ and Iso were both antagonized by propranolol, but not by practolol. These results indicate that TMQ and Iso inhibit the anaphylactic reactions by β-adrenergic mechanisms, probably of a β2-type.

In vitro release of eosinophil chemotactic factor of anaphylaxis (ECF-A) from guinea pig skin.

An in vitro release of the eosinophil chemotactic factor of anaphylaxis (ECF-A) in anaphylactic reactions was studied using skin slices from actively sensitized guinea pigs. ECF-A and histamine were released in vitro from actively sensitized guinea pig skin by antigen challenge. The magnitude of ECF-A release did not always parallel that of anaphylactic histamine release in guinea pig skin, suggesting that there may be no correlation between the amount of ECF-A and that of histamine released from the skin in anaphylactic reactions in guinea pigs.

Inhibition of passive anaphylaxis induced in the rat hind paw and peritoneal cavity by N-(2-oxo-3,5,7-cycloheptatrien-1-yl)-aminooxoacetic acid ethyl ester (AY-25,674).

Passive anaphylaxis induced in the rat hind paw and peritoneal cavity with rat serum containing immunoglobulin E antibody was inhibited by N-(2-oxo-3,5,7-cycloheptatrien-1-yl)-aminooxoacetic acid ethyl ester (AY-25,674). In contrast with disodium cromoglycate (DSCG), AY-25,674 was orally active. Otherwise, the activity profile of AY-25,674 was similar to that of DSCG. Peak activity occurred a short time after administration, large doses produced tachyphylaxis, and anaphylactic histamine release from mast cells was inhibited. AY-25,674 did not inhibit increased vascular permeability produced by nonreaginic antibody, compound 48/80, serotonin, or histamine. It is concluded that AY-25,674 produces its antiallergic effects by inhibiting mediator release from mast cells by a mechanism similar to that of DSCG.

Enhancement of anaphylactic mediator release from guinea-pig perfused lungs by fatty acid hydroperoxides

Fragments of chopped lung from indomethacin treated guinea-pigs had an anti-aggregating effect when added to human platelet rich plasma (PRP), probably due to the production of prostacyclin (PGI 2) since the effect was inhibited by 15-hydroperoxy arachidonic acid (15-HPAA, 10 μg ml −1). Both 15-HPAA (1–20 μg ml −1 min −1) and 13-hydroperoxy linoleic acid (13-HPLA, 20 μg ml −1 min −1) caused a marked enhancement of the anaphylactic release of histamine, slow-reacting substance of anaphylaxis (SRS-A) and rabbit aorta contracting substance (RCS) from guinea-pig isolated perfused lungs. This enhancement was not reversed by the concomitant infusion of either PGI 2 (5 μg ml −1 min −1) or 6-oxo-prostaglandin F 1α (6-oxo-PGF 1α, 5 μg ml −1 min −1). Anaphylactic release of histamine and SRS-A from guinea-pig perfused lungs was not inhibited by PGI 2 (10 ng - 10 μg ml −1 min −1) but was inhibited by PGE 2 (5 and 10 μg ml −1 min −1). Antiserum raised to 5,6-dihydro prostacyclin (PGI 1) in rabbits, which also binds PGI 2, had no effect on the release of anaphylactic mediators. The fatty acid hydroperoxides may enhance mediator release either indirectly by augmenting thromboxane production or by a direct effect on sensitized cells. Further experiments to distinguish between these alternatives are described in the accompanying paper (27).

Mechanism of histamine release from rat mast cells induced by the ionophore A23187: effects of calcium and temperature.

1 The mechanism of histamine release from a pure population of rat mast cells induced by the lipid soluble antibiotic, A23187, has been studied and compared with data for anaphylactic histamine release reported in the literature. 2 Histamine release induced by A23187 in the presence of calcium 10(-3) mol/l was completed in 10 minutes. By preincubation of the mast cells with A23187 for 10 min in the absence of calcium the histamine release induced by calcium, 10(-3) mol/l or 5 x 10(-3) mol/l, was completed in 90 s and 45 s, respectively. 3 A23187-induced histamine release was maximal with calcium 10(-3) mol/l when the cells were incubated at 33 to 39 degrees C for 10 minutes. 4 The cellular mechanism, which was stimulated by A23187 and calcium for the release of histamine, was irreversibly inactivated by incubation at 45 degrees C. 5 An inhibition of energy metabolism was excluded as the cause of the heat inactivation. 6 The dependence of A23187-induced histamine release on calcium and temperature, the time course of histamine release and the heat inactivation are consistent with the view that the same mechanism is involved in A23187-induced and anaphylactic histamine release.

Allergic reactions, cAMP and histamine release. A re-evaluation of the cAMP hypothesis [proceedings

Our experiments were based on direct anaphylactic histamine release in the pure target cell, which is in contrast to other studies with reversed anaphylactic histamine release or with mixed cell populations.