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PubMed1985

Inhibition of histamine release from basophil leucocytes of asthmatic patients treated with corticosteroids.

We studied the protective effect of corticosteroids in asthmatic patients both in vivo and in vitro. Steroid treatment of patients inhibited the in vivo response to bronchial challenge with the specific allergen as shown by the substantial rise in allergen-threshold. It also produced inhibition of the in vitro elicited release of histamine and slow-reacting substance of anaphylaxis from blood leucocytes. This effect was apparent within 24 h of starting treatment with prednisolone in a daily dose of 30 mg, and reached a maximum after 48 h. In addition, in peripheral venous blood basophil count and total leucocyte histamine content were reduced, eosinophils disappeared and neutrophils increased.

Adrenal Cortex Hormones↗

PubMed1983

Membrane potential changes during IgE-mediated histamine release from rat basophilic leukemia cells.

The membrane potential of rat basophilic leukemia cells (RBL-2H3 cell line) has been determined by monitoring the distribution of the lipophilic [3H] tetraphenylphosphonium cation between the cells and the extracellular medium. By this method, the determined potential of these cells, passively sensitized with IgE, is -93 +/- 5 mV (mean +/- SEM, interior negative). Almost 40% of this membrane potential is rapidly collapsed upon the addition of the proton carrier, carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (FCCP). It is suggested that the FCCP-sensitive fraction of the total membrane potential results from the accumulation of this cation by the mitochondria, which maintains a negative membrane potential. Thus, the resting plasma membrane potential of these cells equals -55 +/- 6 mV. During the process of immunological stimulation by antibodies directed against cell membrane bound IgE, the membrane potential decreases. Moreover, there is a correlation between the extent of degranulation of the cells and the depolarization. It is concluded that in common with other secretory systems, depolarization of the plasma membrane is involved in the stimulus-secretion coupling of the histamine secreting RBL cells.

Animals↗

PubMed1992

Hyperosmolarity selectively enhances IgE-receptor-mediated histamine release from human basophils.

Increased osmotic pressure has been reported to cause non-cytotoxic histamine release (HR) from human basophils, as well as a potentiation of HR induced by anti-IgE. In this study, the effects of hyperosmolar Na-K-acetate (300-600 mOsm/kg H2O) on HR was studied in washed human blood cells from newborns, adult volunteers and patients with severe atopic dermatitis. These three patient groups represented 3 very distinct populations with respect to total plasma IgE content, medians were less than 0.2 IU/ml, 20.5 IU/ml and 2508 IU/ml; respectively. Increasing osmolarity to 500 mOsm/kg H2O caused little HR in the absence of other stimuli, whereas at 600 mOsm/kg H2O a significant increase in spontaneous HR was seen. The HR induced by anti-IgE and Concanavalin A, acting through the IgE-receptor, was increased approximately twofold at 500 mOsm/kg H2O. Responses were highly correlated to results at 300 mOsm/kg H2O. The use of 600 mOsm/kg H2O buffers caused a further increase in most, but not all blood samples. The potentiation of IgE-receptor-mediated HR when using hyperosmolar media was clearly independent of plasma IgE contents, and did not change the concentration-response to anti-IgE. In contrast, HR induced by the IgE-receptor-independent stimuli, Formyl-met-leu-phe and calcium ionophore A 23187, were not enhanced at all by increased osmotic pressure. We conclude, that hyperosomolar media selectively enhance IgE-receptor-mediated HR. The use of hyperosmolar media may therefore be beneficial in a diagnostic application of washed blood HR assays used in allergy diagnosis.

Acetates↗

PubMed1994

Direct effects of second-generation H1-receptor antagonists on the activation of human basophils.

The present study was performed to investigate the putative suppressive effects of H1-receptor antagonists (HRA) of the second generation (astemizole (AS), cetirizine (CT), loratadine (LO), oxatomide (OX) and terfenadine (TF)) on the mediator release from human basophils activated by two classical stimuli. Anti-IgE-mediated histamine release was inhibited in a dose-dependent fashion by TF (maximum inhibitory value: 33.8 +/- 7.6%, 100 microM, n = 7), whereas the other HRA exhibited weaker activity. The anti-IgE-induced LTC4 production was strongly suppressed by TF, LO and OX (92.4 +/- 6.3%, 90.8 +/- 6.0% and 88.5 +/- 5.6%, 100 microM, n = 4-5), while AS was less active (56.4 +/- 4.1%, 100 microM, n = 5). Histamine release induced by incubation with grass pollen antigen (0.01%) was inhibited by TF (40.7 +/- 4.1%, 50 microM, n = 4), but the other HRA showed only low activity. The present findings suggest that some HRA might exhibit direct inhibitory effects on activation of IgE-receptor bearing cells.

Basophils↗

PubMed1994

Investigations with the selective PKC inhibitor chelerythrine on human basophils.

Modulation of protein kinase C (PKC) activity in basophils (B) can influence IgE-mediated histamine release (HR). The present study investigated the effects of chelerythrine, which inhibits isolated PKC (IC50 0.7 microM), on different activation pathways in B. Fc epsilon RI-mediated HR was strongly inhibited by chelerythrine (86.5 +/- 5.4%, 5 microM, n = 11). TPA-induced mediator release was also suppressed: 77.1 +/- 8.5% inhibition (7.5 microM). HR due to non-immunological stimuli (A23187, FMLP) was strongly inhibited by chelerythrine. Previously, other selective PKC-inhibitors have been shown to potentiate IgE-mediated HR from B suggesting a negative modulatory role of PKC, whereas non-specific inhibitors such as staurosporine inhibited HR. Chelerythrine might therefore be less selective for PKC. This may be indicated by the fact that chelerythrine inhibits PKC at its catalytic domain, which is homologous with other protein kinases.

Alkaloids↗

PubMed1987

The influence of cimetidine and ranitidine on basophil histamine release and bronchial reactivity in asthmatic patients.

Anti-IgE induced histamine release from isolated basophils after Cimetidine and Ranitidine administration was evaluated in 22 patients with atopic bronchial asthma. The histamine provocation test after Ranitidine treatment in 10 patients with atopic bronchial asthma and 10 patients with peptic ulcer was also performed. Investigations in vitro revealed that Cimetidine and Ranitidine in low concentrations had an inhibitory effect whereas in concentrations of over 10(-6) M and 10(-4) M, respectively, they enhanced histamine release. Investigations in vivo after administration of Ranitidine showed that it does not cause marked changes in the bronchial reactivity in patients with bronchial asthma and any change in patients with peptic ulcer. These preliminary studies seem to suggest that in patients with atopic bronchial asthma and concomitant peptic ulcer Ranitidine is preferable to Cimetidine in the treatment of digestive tract disorders.

Antibodies, Anti-Idiotypic↗

PubMed1988

Effects of phorbol ester, serine phospholipids, and calcium on histamine release from mast cells and basophils.

The effects of calcium, serine phospholipids and the phorbol ester tetradecanoylphorbol acetate (TPA), a known activator of protein kinase C, have been examined on mastocytes from different sources. A complex and differential interaction between these agents and histamine secretion was observed in human basophil leucocytes and in peritoneal mast cells from the rat, mouse and hamster. On this basis, the possible role of kinase C in histamine release is discussed.

Animals↗

PubMed1989

Studies of the mechanism of desensitization of anti-IgE-mediated histamine release from human basophils.

Human basophils became hyporesponsive to anti-IgE when exposed to this agent in the absence of Ca2+ for more than 10 min. The desensitization process proceeded in parallel to the releasing-process. The mechanism of desensitization seems to involve a very early step in the release-reaction, since the response to phospholipase A2 and diolein, agents involved in the release-reaction, was not affected by the desensitization.

Antibodies, Anti-Idiotypic↗

PubMed1989

Influenza A virus enhances IgE-mediated histamine release from human basophil leukocytes. Examination of the effect of viral neuraminidase and haemagglutinin.

Histamine release caused by anti-IgE was examined in leukocyte suspensions from 10 healthy individuals. Influenza A virus was found to enhance the histamine release but did not release histamine per se. When monoclonal antibodies directed against the viral neuraminidase were included in the samples, the potentiating effect of the virus was completely abolished. The same occurred using a neuraminidase inhibitor. However, monoclonal antibodies directed against the viral haemagglutinin also abolished the potentiation. A binding of virus to the basophil cell surface by haemagglutinin therefore seems to be necessary for the viral neuraminidase to cause potentiation of mediator release.

Antibodies, Anti-Idiotypic↗

PubMed1989

Effects of antihistamines on isolated human lung mast cells, basophil leucocytes and erythrocytes.

Low concentrations of H1- and H2-receptor directed compounds inhibited the immunologic secretion of histamine from human lung mast cells and basophil leucocytes and protected human erythrocytes from hypotonic lysis. Higher concentrations induced a release of the amine from the histaminocytes. These results are discussed in terms of the possible membrane effects of the test compounds.

Basophils↗

PubMed1996

The characterization of tyrosine phosphorylation of 78 and 92 kDa proteins in rat basophilic RBL-2H3 cells.

Previously, we have demonstrated that tyrosine phosphorylation of 78 and 92 kDa proteins in rat basophilic leukemia cells (RBL-2H3) is involved in a signal transduction system for high-affinity IgE receptor (Fc epsilon RI)-mediated histamine secretion. However, it is not clarified whether the tyrosine phosphorylation of 78 and 92 kDa proteins in RBL-2H3 cells is regulated by activation of protein kinase C (PKC) or phosphatidylinositol 3-kinase (PI3-kinase). In this study, therefore, the effect of depletion of PKC in RBL-2H3 cells, or the influence of PKC, PI3-kinase and tyrosine kinase inhibitors on histamine release from RBL-2H3 cells was examined. The elimination of PKC in RBL-2H3 cells induced significant suppression of histamine release, although the tyrosine phosphorylation of 78 and 92 kDa proteins was not inhibited. The inhibition of histamine release was also observed by the treatment with a PKC inhibitor such as H-7, calphostin C, a PI3-kinase inhibitor such as wortmannin or a tyrosine kinase inhibitor such as ST638, genistein, hervimycin A, although the tyrosine phosphorylation of both proteins was inhibited by only ST638. These results suggest that the 78 kDa protein in RBL-2H3 cells is not identical to the protein-tyrosine kinase PTK72 and the tyrosine phosphorylation of 78 and 92 kDa proteins in RBL-2H3 cells occurs upstream of PKC and PI3-kinase activation or is regulated independently of the PKC- and PI3-kinase-dependent signaling pathway.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMedDate not supplied

Rheology of rat basophilic leukemia cells.

Rat basophilic leukemia (RBL) cells, decorated with IgE, have been shown to bind irreversibly to antigen-coated substrates. In this paper we measured RBL cell deformability and demonstrated that this irreversible binding is not due to a compliant cellular rheology of these cells. The rheological properties of RBL cells were assessed with single-cell micropipette aspiration. Small-sized (G1/G0 phase) cells were found to be more deformable than medium-sized (S phase) cells. No changes in cellular rheology were observed after binding of anti-dinitrophenol IgE to Fce receptors. Furthermore, cytoplasmic viscosity mu showed power-law dependence on mean shear rate gama m: mu = mu c(gamma m/gamma c)-b, where mu c is a characteristic viscosity at characteristic shear rate gamma c, and b is a material coefficient. All the cells exhibited similar dependence on shear rate (b approximately 0.5). When gamma c was set to 1 s-1. mu c = 480 +/- 10,560 +/- 40 and 490 +/- 10 Pa.s for G1/G0, S cells, and G1/G0 cells treated with the antibody, respectively. In general. RBL cells were much more rigid than normal neutrophils (mu c = 130 +/- 20 Pa, s b = 0.5). Thus the biochemistry of the adhesion molecules, not the cellular deformability of the cell, is the cause of the irreversibility of RBL cell adhesion under flow.

2,4-Dinitrophenol↗

PubMedDate not supplied

Adenosine-adenosine deaminase modulation of histamine release from human basophils in vitro.

Since extracellular adenosine is a physiologically important regulator of adenylate cyclase and cell function in various mammalian tissues, we have examined the effect of adenosine on histamine release from human basophils. Adenosine inhibited IgE-mediated histamine release by its ability to increase leukocyte cyclic AMP levels; the same concentrations of adenosine which inhibited histamine release increased the cyclic AMP level of mixed leukocytes. Inhibition of histamine release was also observed with an adenosine deaminase (ADA) inhibitor [erythro-9-(2-hydroxy-3-nonyl)-adenine: EHNA] in the presence of autologous serum. We suggest that the adenosine-ADA system normally modulates histamine release and that this contributes to the severe combined immune deficiency (SCID) associated with a lack of ADA.

Adenosine↗

PubMed1998

Ca2+-dependent capacitance increases in rat basophilic leukemia cells following activation of store-operated Ca2+ entry and dialysis with high-Ca2+-containing intracellular solution.

Ca2+-dependent vesicular fusion was studied in single whole-cell patch-clamped rat basophilic leukemia (RBL) cells using the capacitance technique. Dialysis of the cells with 10 microM free Ca2+ and 300 microM guanosine 5'-O-(3-thiotriphosphate) (GTP[gamma-S]) resulted in prominent capacitance increases. However, dialysis with either Ca2+ (225 nM to 10 microM) or GTP[gamma-S] alone failed to induce a capacitance change. Under conditions of weak Ca2+ buffering (0.1 mM EGTA), activation of Ca2+-release-activated Ca2+ (CRAC) channels by dialysis with inositol 1,4,5-trisphosphate (InsP3) failed to induce a capacitance increase even in the presence of GTP[gamma-S]. However, when Ca2+ATPases were inhibited by thapsigargin, InsP3 and GTP[gamma-S] led to a pronounced elevation in membrane capacitance. This increase was dependent on a rise in intracellular Ca2+ because it was abolished when cells were dialysed with a high level of EGTA (10 mM) in the recording pipette. The increase was also dependent on Ca2+ influx because it was effectively suppressed when external Ca2+ was removed. Our results demonstrate that ICRAC represents an important source of Ca2+ for triggering a secretory response.

Animals↗

PubMed1997

Loss of cell surface microvilli on rat basophilic leukaemia cells precedes secretion and can be mimicked using the calmodulin antagonist trifluoperazine.

OBJECTIVE: We studied changes in cell surface morphology following treatment with secretagogue or trifluoperazine in a mast cell model. MATERIALS AND METHODS: Rat basophilic leukaemia (RBL) cells were treated with antigen and or the calmodulin antagonist, 0-50 microM trifluoperazine (TFP). The release of a secretory granule enzyme, beta-hexosaminidase, into the external medium was used as a measure of secretion. Quantitation of cell surface microvilli was determined by using a computer with input from a digitising tablet from scanning electron micrographs. Cytoskeletal proteins present in microvilli were analysed by confocal immunofluorescence. RESULTS: When RBL cells are stimulated to secrete with an antigen, the cell surface is transformed from a microvillous morphology to a ruffled one. The cell surface rearrangement preceded beta-hexosaminidase secretion: the majority of microvilli disappeared rapidly after stimulation (t1/2 of 39 s) whereas secretion can only be measured after a lag of 47 s. The calmodulin antagonist, TFP did not inhibit antigen-induced secretion or loss of microvilli, however TFP alone caused a similar loss of microvilli but was unable to stimulate or potentiate secretion. The microvilli mostly disappeared within 30 s, and a half-maximal effect occurred at approximately 8 microM TFP. Using immunofluorescence, calmodulin was localized to punctate structures on the dorsal cell surface which presumably correspond to the microvilli, and which also stained for F-actin and myosin I. CONCLUSIONS: Loss of cell surface microvilli on RBL cells precedes secretion and could reflect a cytoskeletal rearrangement which facilitates fusion of secretory granules with the membrane. It can be mimicked using trifluoperazine and we suggest it may involve calmodulin-binding components of the microvillus cytoskeleton such as myosin I.

Animals↗

PubMed2005

[Basophil activation tests in the diagnosis of drug reactions].

Over the past 10 years a number of studies on basophil activation tests (BAT) have been published which focus on their use as diagnostic methods in clarifying IgE-mediated hypersensitivity reactions to various allergens including drugs. These BAT are based on flow cytometric quantification of allergen- induced CD63 or CD203 expression or measurement of sulfo leukotriene release by ELISA. In the diagnosis of penicillin allergy, the combined use of the CD63-BAT and specific IgE increases sensitivity. The role of BAT in the diagnosis of non-IgE-mediated reactions to non-steroidal anti- inflammatory drugs remains to be clarified. This article focuses on (1) the principles of BAT, (2) technical aspects, (3) clinical applications and (4) recommendations for further development.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1996

A Ca2+ current activated by release of intracellular Ca2+ stores in rat basophilic leukemia cells (RBL-1).

We have characterized a Ca2+ current activated by depletion of intracellular Ca2+ stores (capacitative Ca2+ entry current) as a first step to investigate the mechanisms underlying communication between the intracellular Ca2+ stores and the plasma membrane Ca2+ permeability. Whole cell currents in response to voltage ramps from -125 to +60 mV from a holding potential of -40 mV were recorded in rat basophilic leukemia cells (RBL-1 cells) in solutions designed to optimize detection of a Ca2+ current. An inwardly rectifying current could be activated upon dialysis of the cell interior with pipette solutions devoid of Ca2+ and containing 20 mm BAPTA, a procedure expected to passively deplete intracellular Ca2+ stores. The current was maximally activated within 2 min, was sensitive to extracellular Ca2+ concentration and was abolished by removal of extracellular Ca2+. The current was markedly reduced in the presence of Ni2+ or La3+. The pathway activated by this protocol was permeant to Ba2+, displaying complex permeability characteristics at negative potentials. A small inward Mn2+ current consistent with a finite permeability of the pathway to Mn2+ was detected. In contrast Ni2+ displayed no detectable current carrying ability. Extracellular Na+ permeated the pathway in the absence of extracellular Ca2+. Under conditions designed to reduce passive depletion of intracellular Ca2+ stores, a Ca2+ current indistinguishable from that described above was activated by addition of ionomycin. This observation is consistent with the activation of the Ca2+ influx pathway occurring as a result of events associated with depletion of intracellular Ca2+ stores. Importantly, application of extracellular Ni2+ in the presence of ionomycin irreversibly inhibited the current. The presence of an inwardly rectifying K+ current in RBL cells could confound studies of the capacitative Ca2+ entry current when recorded using pipette solutions devoid of K+ since this current would be inward over the voltage range used to investigate the capacitative Ca2+ entry current. This study compares an inward rectifying K+ current and the capacitative Ca2+ entry current in RBL cells and highlights some similarities and differences between the two currents. The results demonstrate that caution should be exercised in interpreting recordings made using extracellular solutions containing even modest amounts of K+ when studying the capacitative Ca2+ entry current in RBL cells.

Animals↗

PubMed1999

Transitional changes in membrane potential and intracellular [Ca2+] in rat basophilic leukemia cells.

Using whole-cell current-clamp measurements we have found that thapsigargin-mediated activation of store-regulated Ca2+ entry in rat basophilic leukemia cells is accompanied by complex changes in membrane potential. These changes consisted of: (i) an initial slow, small depolarization, (ii) a transitional change in potential to a depolarized value and (iii) transitional changes between a hyperpolarized and a depolarized potential. These complex changes in potential can be explained by the interaction between the endogenous inwardly rectifying K+ conductance and the generation of a small inward current. To investigate the possible influence of these changes of potential on [Ca2+]i, single cell measurements of fura2 fluorescence were undertaken alone or in combination with current-clamp measurements. Thapsigargin-mediated activation of the store-regulated Ca2+ entry pathway was accompanied by a marked increase of [Ca2+]i. During this increase, transient, abrupt declines in [Ca2+]i were detected in approximately 60% of the cells investigated. These changes of [Ca2+]i are consistent with the observed changes of membrane potential recorded under current-clamp.

Animals↗