Comparison of histamine and serotonin release from rat peritoneal mast cells induced by nerve growth factor and compound 48/80

Inflammation Research -     

Effect of sensitization and non-antibody IgE on 48/80 induced histamine release from isolated rat mast cells

Histamine release from isolated rat mast cells from non-immunized and immunized Hooded Lister rats was induced by compound 48/80. The histamine release was decreased with a lower maximum at the optimal concentration of 48/80 when using cells from immunized rats compared to non-immunized control rats. The stimulation of IgE antibody production, after immunization using B. pertussis as an adjuvant was also accompanied by an elevation of total serum IgW. The 48/80 induced histamine release from Sprague Dawley mast cells was not inhibited by immunization. Non-antibody IgE showed a non-competitive inhibition of 48/80 induced histamine release when myeloma IgE was incubated with mast cells from both Hooded Lister and Sprague Dawley rats. The results indicate the existence of different receptors for IgE and 48/80.     

Total serum IgE influence on the anaphylactic and 48/80 induced histamine release from isolated rat mast cells

We have investigated the influence of non-specific IgE on histamine release induced by antigen or compound 48/80. Our results indicate that increased amounts of IgE influence antigen mediated histamine release as well as release induced by a non-immunological stimulus like compound 48/80.     

Broncho-Vaxom® inhibits histamine release from rat mast cells induced by compound 48/80 and ionophore A23187

Broncho-Vaxom (BV) inhibited in dose-dependent manner the release of histamine from and degranulation of isolated rat peritoneal mast cells stimulated with compound 48/80 and the ionophore A23187. Inhibition persisted after removal of BV from the incubation medium before stimulation, but did not occur when bovine serum albumin (BSA) was used instead of BV. Binding of BV to mast cells was observed by electron microscopy on cells that had been incubated with colloidal-gold labelled BV. There was no significant difference between the binding of BV gold and BSA gold to the mast cells. Washing before fixation removed most of the BV gold from the cells. This study establishes BV as anin vitro histamine release inhibitor.     

Inhibition by Triton X-100 of histamine liberation from mast cells induced by substance 48/80

Triton X-100, in concentrations below those liberating histamine, produced dose-dependent inhibition of histamine liberation from rat mast cells induced by substance 48/80. Triton X-100 (0.02 ml/liter) exhausted the ATP reserves in the mast cells and completely inhibited histamine liberation induced by substance 48/80, and exhaustion of the ATP content in the mast cells was abolished by glucose (10 mM). It was concluded that inhibition by Triton X-100 of histamine liberation induced by substance 48/80 depends on the inhibition of energy production.Allergologic Research Laboratory, Academy of Medical Sciences of the USSR, Moscow, Department of Pharmacology, Kuban Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. D. Ado.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 2, pp. 185–187, February, 1979.     

Ca-dependent and Ca-independent histamine release from mast cells induced by active components of compound 48/80

Compound 48/80 and 14C-labelled compound 48/80 were synthesized, and fractionated by thin-layer chromatography into 14 components with various histamine-releasing activities and different Ca++ requirements for their actions. The histamine release induced from rat mast cells in vitro by the most active component, fraction D (molecular weight = 2280, a tridecamer composed of 13 monomer units), was greatly elevated by extracellular Ca++, and was partially reduced by pretreatment of the cells with dinitrophenylated Ascaris antiserum, an IgE. In contrast, the histamine release induced by fraction H (molecular weight = 1580, a nonamer composed of 9 monomer units), was higher in Ca-free medium than in Ca-containing medium, and partially suppressed by pretreatment of mast cells with neurotensin or substance P, both Ca-independent releasers. The binding potencies of the 14C-labelled components estimated at 4 degrees C in the presence of Ca++, where no degranulation of the cells occurs, generally paralleled their histamine-releasing activities. However, Ca++ was inhibitory for the binding of 14C-fraction H. The binding of fraction D to [3H]arachidonic-acid-preloaded mast cells induced a rapid accumulation of the labelled arachidonic acid into phosphatidic acid, phosphatidylinositol and phosphatidylcholine, with concomitant decrease of the labelled arachidonic acid from phosphatidylethanolamine prior to the detectable histamine release.     

Mechanism of histamine release from rat peritoneal mast cells

Summary The present communication endeavours to elucidate the mechanism of histamine release from rat peritoneal mast cells induced by selective histamine liberators.Of the different enzymatic processes involved in secretion the following are considered: ecto-ATPase activity in the mast cell, pro-esterase-esterase conversion during histamine secretion, cyclic AMP and microtubule association/dissociation, phospholipase A₂ and the effect of phospholipid metabolites on secretion, N-methyl transferase and the methylation of phospholipids and the phosphorylation and desphosphorylation of proteins.     

Juxtacellular histamine concentration governs histamine release from rat peritoneal mast cells

Isolated rat peritoneal mast cells release histamine when superfused with isoosmotic salt or sucrose solutions. The release was ascribed by us to an intracellular ion exchange between potassium and histamine at granule sites, resulting from a flux of cytoplasmic potassium across the granules secondary to the disturbance of the ‘state of equilibrium’ at the cell surface caused by the superfusion (Uvnäs et al. 1989). In the present article is shown that the histamine releasing effect is counteracted by the addition of histamine to the superfusion fluid. The inhibition is concentration-dependent and accompanied by concomitant changes in the potassium efflux. A 50% inhibition of the histamine release requires an external histamine concentration of 40 μm and extrapolation of the equilibrium curve hints at a total inhibition at concentrations around 170 μm. The observations are taken to indicate that reduction of the juxtacellular histamine concentration caused by the superfusion disturbs the histamine equilibrium at the mast cell surface resulting in the activation of the histamine secretory mechanism. In other words, the secretory activity of the mast cell is checked by the juxtacellular concentration of histamine. When the juxtacellular histamine is removed e.g. on isolation procedures, other experimental situations such as superfusion, or by consumption in vivo the mast cell delivers histamine to restore the juxtacellular equilibrium.     

Prostaglandin and histamine release from stimulated rat peritoneal mast cells

The production of five prostanoids (PGD₂, PGE₂, PGF₂, 6-oxo-PGF₁, and TxB₂) was examined after mast cell activation. Prostaglandin D₂ (PGD₂) was the major prostanoid produced after stimulation of rat peritoneal mast cells with the calcium ionophore A 23187, compound 48/80 or anti-rat IgE. The amount of PGD₂ generated was not dependent on the quantity of histamine released. The time course of PGD₂ production paralleled the release of histamine following activation with A 23187 or anti-rat IgE but with compound 48/80 release of histamine reached a maximum within 15 sec, whereas production of PGD₂ was apparent only after 5 min and was still increasing at 30 min.     

Characteristics of histamine and serotonin release from rat mast cells induced by thymic peptides

Thymopoietin peptides release histamine and serotonin from rat mast cells. The release has the characteristics of other basic secretagogues in that it occurs rapidly, does not require extracellular Ca²⁺ ions, and is inhibited by benzalkonium chloride (BAC). These similarities indicate that chemically different basic compounds have common mechanisms for histamine and serotonin release from rat mast cells.     

Mechanisms of vancomycin-induced histamine release from rat peritoneal mast cells

The mechanisms of vancomycin (VCM)-induced histamine release were studied with rat peritoneal mast cells. VCM (>1×10^–3 M) released histamine from the isolated mast cells in a dose-dependent and noncytotoxic manner. In the absence of extracellular Ca²⁺, the histamine release was reduced markedly. When the intracellular Ca²⁺ was depleted, it was further decreased. The Fura-2-loaded single mast cells showed a biphasic increase in the intracellular Ca²⁺ concentration ([Ca²⁺]_i) by VCM: the first transient and the second sustained components. In the absence of extracellular Ca²⁺, the transient component was unchanged, while the sustained component was eliminated completely. The IP₃ content in the mast cells increased within 10 s after the application of VCM. These results suggest that VCM releases histamine from rat peritoneal mast cells via an IP₃ production and increase in [Ca²⁺]_i.     

Further characterisation of substance P induced histamine release from human bronchoalveolar lavage mast cells

Inflammation Research -     

The effect of some anti-inflammatory drugs on histamine and serotonin release from rat peritoneal mast cells

Inflammation Research -     

Juxtacellular histamine concentration governs histamine release from rat peritoneal mast cells.

Isolated rat peritoneal mast cells release histamine when superfused with isoosmotic salt or sucrose solutions. The release was ascribed by us to an intracellular ion exchange between potassium and histamine at granule sites, resulting from a flux of cytoplasmic potassium across the granules secondary to the disturbance of the 'state of equilibrium' at the cell surface caused by the superfusion (Uvn?s et al. 1989). In the present article is shown that the histamine releasing effect is counteracted by the addition of histamine to the superfusion fluid. The inhibition is concentration-dependent and accompanied by concomitant changes in the potassium efflux. A 50% inhibition of the histamine release requires an external histamine concentration of 40 microM and extrapolation of the equilibrium curve hints at a total inhibition at concentrations around 170 microM. The observations are taken to indicate that reduction of the juxtacellular histamine concentration caused by the superfusion disturbs the histamine equilibrium at the mast cell surface resulting in the activation of the histamine secretory mechanism. In other words, the secretory activity of the mast cell is checked by the juxtacellular concentration of histamine. When the juxtacellular histamine is removed e.g. on isolation procedures, other experimental situations such as superfusion, or by consumption in vivo the mast cell delivers histamine to restore the juxtacellular equilibrium.     

Auranofin inhibits histamine release from rat peritoneal mast cells.

The effect of auranofin on histamine release from immunologic and non-immunologic activated rat peritoneal mast cells cocultured with 3T3 fibroblasts (MC/3T3) was investigated. When MC/3T3 were preincubated with 2 x 10(-5) M auranofin and thereafter challenged with anti-IgE antibodies, a maximal inhibition of histamine release (86.2%) was obtained. Non-immunological histamine release induced by compound 48/80, substance P and bradykinin was inhibited to a lesser degree, i.e. 36.0%, 37.6% and 24.0% respectively. Simultaneous incubation of auranofin and the stimulating agents resulted in a higher inhibition of histamine release: anti-IgE antibodies--92.0%; compound 48/80--73.5%; substance P--46.1%. We conclude that auranofin effectively reduces histamine release from immunologic and non-immunologic activated mast cells. This may be relevant to the control of allergic reactions.     

A toxic substance from the sea urchinToxopneustes pileolus induces histamine release from rat peritoneal mast cells

A toxic substance (P-II fraction), fractionated from the pedicellariae of the sea urchinToxopneustes pileulus, dose-dependently caused the histamine release from rat peritoneal mast cells. The histamine release induced by P-II fraction increased with time, while compound 48/80 caused a more rapid histamine release. The dose-response curve for P-II fraction was studied with concentration 0.03–2.0 mg/ml. This reaction was dependent on Ca²⁺ and temperature. When glucose (5.5. mM) was omitted during the incubation step, the histamine release induced by P-II fraction was significantly reduced as compared to that of compound 48/80. Pyruvate reversed this reduction. On the other hand, the histamine release induced by P-II fraction was effectively potentiated by the addition of glucose (11.0 mM), but not that by compound 48/80. These results suggest that P-II fraction-induced histamine release differs from that of compound 48/80 disregards to the effects of glucose, because this histamine release appears to be more sensitive to the glycolytic pathway than compound 48/80-induced histamine release.