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PubMed1977

Experiments on the passive sensitization of human basophils, using quantitative immunofluorescence microscopy.

In previous experiments a correlation was found between the amount of IgE on human basophils and the IgE serum level. The results of these experiments are shown to fit a free exchange model with an approximately constant K-value. We investigated whether the free IgE-receptors on the basophils, which should be present according to this model, could be saturated by incubating the cell suspensions with IgE myeloma protein or with sera from patients with an elevated IgE serum level. Various incubation conditions were applied in sensitizing the leukocytes, and cells from both atopic and nonatopic subjects were used for testing, but no increase in basophil-bound IgE could be measured with the quantitative immunofluorescence technique. Nor could we demonstrate a significant dissociation of cell-bound IgE in a period of 24 h. Therefore another hypothesis is put forward, in which receptor turnover is taken into account: we assumed that that free receptors on the basophils had a shorter functional half-life, than the half-life of the IgE-receptor complexes. This model would explain the contradictory results mentioned above.

Basophils↗

PubMed1977

Cell-bound IgE on human mast cells and basophilic granulocytes in atopic and nonatopic subjects.

In previous studies basophil-bound IgE was measured by means of quantitative immunofluorescence miscroscopy. But mast cells are of particular importance in local atopic reactions, we thought it necessary to investigate the IgE-load on both cell types. The amount of mast cell-bound IgE can be estimated in a semiquantitative way by end point titration with a fluoresceinated sheep antihuman IgE (FlaIgE). The amount of mast cell-bound IgE was estimated this way in tonsils, adenoids, bronchial and tracheal tissues, and was compared with the amount of IgE on the basophils. A correlation was found between the IgE-load on mast cells and on basophils. Atopic patients had a higher mast cell fluorescence titer (MCFT) than nonatopic controls. It was demonstrated that, as on basophils, the IgE level of the serum contributes to this difference.

Basophils↗

PubMed1977

Electron microscopic studies on human basophils from atopic and nonatopic subjects, using horse radish peroxidase labelled anti-IgE.

In previous studies, quantitative differences in cell-bound IgE on the basophils from various donors were measured by means of a quantitative immunofluorescence technique. In this study, cell-bound IgE was demonstrated on basophilic granulocytes by immunoelectron microscopy, using horse radish peroxidase labelled anti-IgE. The distribution of IgE on the basophils was studied in both atopic and nonatopic subjects. The intensity of the peroxidase staining on the basophils varied and appeared to correlate with the amount of cell-bound IgE, as estimated by quantitative immunofluorescence.

Antibodies, Anti-Idiotypic↗

PubMed1978

Quantitation of IgE on the basophil surface in atopic patient.

A radioimmunoassay was employed in order to quantitate IgE on the basophil surface in 6 normal and 10 pollen sensitive subjects. A basophil-rich fraction obtained from whole blood in a Ficoll gradient was incubated with specific anti-IgE; the inhibition produced by surface IgE was standard inhibition curve. Atopic patients had on the average about 10-30 times as many IgE molecules per basophil as control subjects. Total and specific IgE as well as degranulation by Lollium perenne crude extract were also studied in both populations and their results compared with those of basophil IgE quantitation.

Basophils↗

PubMed1984

In vitro antigen-induced increase in motility and degranulation of basophilic granulocytes from atopic asthmatics, studied by microscopic motion pictures.

Increase in motility and degranulation of basophilic granulocytes by stimulation with antigen were studied by phase-contrast microscopic motion pictures. There was no difference in random movement between sensitized (atopic asthmatics) and nonsensitized basophilic granulocytes (healthy subjects). The incidence of basophilic granulocytes with oriented movement before antigen stimulation was significantly lower in atopic asthmatics compared to that in healthy subjects, but was significantly increased at 3-6 min and reached the peak at 12-15 min after addition of antigen. Degranulation of sensitized basophilic granulocytes began to occur at 3-6 min with the maximum at 12-15 min after antigen stimulation.

Asthma↗

PubMed1985

Unique features of human basophilic granulocytes developed in in vitro culture.

Human basophilic granulocytes were obtained in suspension culture of mononuclear cells from umbilical cord blood. Precursors of basophils in the cord blood are nonadherent cells and bear neither surface Ig nor T cell marker. Cultured basophils contain chondroitin-4-sulfate proteoglycan, 1.74 micrograms histamine per 10(6) cells in average, and bear 120,000-380,000 IgE receptors per cell. The IgE receptor molecule has a molecular weight of approximately 64,000 daltons. Human, rat and mouse IgE bind to the receptors with comparable high affinity and passively sensitize the cells for mediator release. Challenge of sensitized basophils with anti-IgE resulted in stimulation of phospholipid methylation, 45Ca uptake, release of both histamine and free arachidonic acid, and enhancement of phosphatidylinositol (PI) turnover. Evidence was obtained that the activation of membrane-associated proteolytic enzyme and methyltransferases is involved in subsequent IgE-mediated biochemical cascades such as PI turnover, Ca2+ uptake and mediator release.

Antibodies, Anti-Idiotypic↗

PubMed1988

Role of IgG4 in histamine release from human basophil leucocytes. I. Sensitization of cells from normal donors.

Several conflicting reports on the ability of IgG4 to mediate type I allergic reactions have appeared lately. We have developed a model system for testing this possibility, using passive sensitization of basophil leucocytes from normal individuals. At first, the system was optimized with regard to donor cells and anti-IgG4 antibody: among 3 normal individuals with cells showing high, medium and low responses to anti-IgE, only the high responder showed a reproducible, but low response to anti-IgG4. This response was consistent when testing anti-IgG4 from different sources, and could be potentiated by a phorbol ester TPA, although not up to the level of anti-IgE. The cells from the high responding donor and a monoclonal anti-IgG4 were selected for further studies. Serum pools from patients allergic to house dust mite (Dermatophagoides pteronyssinus) were used for passive sensitization. The pools contained allergen-specific IgE with or without concomitant IgG4 of the same specificity. The sensitized basophils reacted to anti-IgE and allergen, but to anti-IgG4 only to a small extent. However, when these serum pools were fractionated by affinity chromatography, only the IgE fractions and not the IgG4 fractions made the cells reactive towards specific allergen. It was still possible to elicit a reaction by triggering IgE with anti-IgE, whereas only a small reaction was seen, when IgG4-sensitized basophils were provoked with anti-IgG4. We conclude that IgG4 does not sensitize normal basophils.

Basophils↗

PubMed1989

Decreased releasability of basophils from patients with cold urticaria after cold exposure.

Histamine release from peripheral blood basophils challenged with C5a, f-met-peptides and calcium ionophore was studied in patients with cold urticaria before and after exposure to low environmental temperatures. Compared to healthy controls, stimulated mediator release before cold exposure was increased in 7 of 11 patients. When challenged by cold exposure mediator release from in vitro-stimulated basophils was decreased. This decrease was more pronounced after stimulation with receptor-mediated stimuli (e.g. C5a) as compared to receptor-unrelated stimuli, e.g. calcium ionophore. In 4 of 11 patients stimulated mediator release before cold exposure was moderately increased. Also after cold exposure only a weak decrease of stimulated histamine release was seen. Levels of activated complement components (C3a) before and after cold exposure failed to provide evidence for complement activation in vivo. Also the number of circulating basophils as well as their cellular histamine content remained normal after cold exposure. The results show that in these patients release of histamine is altered before and after cold exposure. These changes in basophil responsiveness are not due to complement activation in vivo.

Basophils↗

PubMed1989

Receptor-operated, but not voltage-operated, calcium channels are involved in basophil leucocyte activation and histamine release.

Transmembrane calcium flux is a critical step in basophil and mast cell activation and subsequent histamine release. This calcium flux is likely to take place through specialized membrane ion channels. Two types of calcium channels have been described so far: the first type is voltage operated and the second type is receptor operated. Depolarization of cell membrane by K+-rich solutions is followed by voltage-operated channel opening in excitable cells, such as smooth muscle cells. We evaluated whether high K+ extracellular concentrations can trigger basophil activation and histamine release. We found that human basophil leucocytes, showing a normal response to activating signals, such as anti-IgE antiserum and formylmethionine peptide, release no histamine when exposed to K+-rich media, alone or in combination with the K+ carrier valinomycin. These results are consistent with there being receptor-operated, but not voltage-operated, calcium channels in the basophil leucocyte plasma membrane.

Basophils↗

PubMed1990

Substance P-induced histamine release from human basophils, skin and lung fragments: effect of nedocromil sodium and theophylline.

We compared histamine release induced by substance P with those obtained with classical secretagogues on human basophils, lung and skin fragments. We also tested the capacity of nedocromil sodium and theophylline to inhibit histamine release in these 3 experimental models. Substance P (10(-4) M) caused a noncytotoxic histamine release (about 10% of total) from basophils, lung and skin fragments. Substance P-induced histamine release was always smaller than that obtained with optimal doses of anti-IgE, formyl-methionine phenylalanine or compound 48/80. Nedocromil sodium did not prevent secretagogue-induced histamine release from basophils or sliced skin. In contrast, it significantly inhibited anti-IgE- or substance P-induced histamine release from human lung. Theophylline caused a dose-related inhibition on these 3 models. We conclude that substance P is a modest secretagogue for human basophils and mast cells, and that skin and lung mast cells are heterogeneous with respect to their response to nedocromil sodium.

Adult↗

PubMed1990

Histamine release from basophils after in vivo application of recombinant human interleukin-3 in man.

Interleukin 3 (IL3) is known to stimulate progenitor cell proliferation and maturation as well as differentiated cell functions, e.g. direct or anti-IgE-mediated histamine release (HR). We investigated 14 patients with malignant diseases being treated with recombinant human IL3 (rhuIL3) as a daily subcutaneous bolus injection for 15 days. For analysis, patients were combined in a 'low-dose' [30 (n = 1), 60 (n = 3) and 125 (n = 2) micrograms/m2/day] and a 'high-dose' [250 (n = 6) and 500 (n = 2) micrograms/m2/day] therapy group. In the high-dose group there was a 2-fold increase in total leukocytes, and 8-fold increase in basophils, and a 23-fold increase in eosinophils. Histamine content per basophil decreased rapidly after rhuIL3 administration. Anti-IgE-induced HR increased in a dose-dependent manner after rhuIL3 therapy (low-dose group: HRmax 47.5 vs. 53.3%; high-dose group: HRmax 57.8 vs. 75.4%, p less than 0.05). In contrast to anti-IgE-induced HR, HR with ionophore (78.0 vs. 50.3%, p less than 0.05), FMLP (32.3 vs. 11.4%, p less than 0.05), sodium chloride (31.8 vs. 22.6%, n.s.) and mannitol (56.3 vs. 47.8%, n.s.) decreased. There was no histamine release from basophils upon in vitro stimulation with rhuIL3 alone. The kinetics of the increase in anti-IgE-induced histamine release did not parallel the rapid histamine depletion of cells. We conclude that rhuIL3 therapy may cause a rapid HR from basophils which cannot be observed after stimulation of cells in vitro. The clinical importance of this HR remains unclear as side effects could not be correlated with HR.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1990

Differential effect of hypertonicity on FMLP-, anti-IgE- and Ca2+ ionophore A23187-induced histamine release from human basophil leukocytes.

Effects of different extracellular Na+ and K+ concentrations (respectively, 135, 155, 220, 260 mM NaCl, and 2.7, 20, 50, 100 mM KCl) on IgE-dependent and IgE-independent histamine release from human basophils were examined. High extracellular Na+ and K+ concentrations were shown to reduce N-formyl-methionyl-leucyl-phenyl-alanine- (FMLP), but not anti-IgE- or Ca2+ ionophore A23187-induced histamine release. A high extracellular Ca2+ (7.2 mM CaCl2) concentration increased basophil response to anti-IgE and FMLP. The enhancement of FMLP- but not of anti-IgE-induced histamine release was antagonized by high extracellular Na+ and K+ concentrations. When leukocytes were suspended in isotonic choline chloride solutions (choline is a nonpermeant monovalent cation), an enhancement of anti-IgE- and FMLP-induced histamine release was observed. This suggests that monovalent cations, namely Na+ ions, at physiological concentrations, downregulate histamine release from human basophils. At high choline chloride concentrations, FMLP-, but not anti-IgE-induced histamine release was inhibited. Thus, the reduction of FMLP-evoked histamine secretion from human basophils seems to be due to hypertonicity and not to the type of monovalent cation, either permeant or nonpermeant, contained in extracellular milieu. The different effects of a hypertonic solution on anti-IgE and FMLP-induced histamine release are probably related to the different cell activation pathways triggered by the two stimuli.

Adolescent↗

PubMed1991

Changes in filament actin accompanying IgE-dependent and -independent histamine release from IL-3-dependent cultured human basophils.

When cord blood mononuclear cells were cultured in the presence of rhIL-3 for 5 weeks or more, 40-90% of cultured cells became morphologically mature basophils. We analyzed the kinetics of histamine release, changes in filament actin (F-actin), and movement of intracellular Ca2+ ([Ca2+]i) induced by IgE-dependent (anti-IgE) and -independent (fMLP) stimuli in these cultured basophils. Anti-IgE and fMLP released 24.5 +/- 5.4% and 14.5 +/- 4.5% histamine from the cells, respectively. Anti-IgE caused actin polymerization with a peak response at 15 min, which began much later than the elevation of [Ca2+]i. In contrast to anti-IgE stimulation, fMLP induced rapid actin polymerization with a peak response at 30 s in correlation with kinetics of histamine release. Our results indicate that cord blood-derived cultured basophils show similar cell functions to mature basophils, and are useful models with which to investigate the mechanisms of degranulation, specifically when a large amount of highly purified cells are required.

Actins↗

PubMed1994

Activated human basophils contain histamine in cytoplasmic vesicles.

Human basophils in contact allergy empty granules slowly--a secretory process termed piecemeal degranulation in contrast to the explosive extrusion of granules seen in anaphylactic degranulation. An ultrastructural enzyme-affinity method to detect histamine, employing diamine oxidase coupled to gold, was used to localize this proinflammatory mediator in human basophils stimulated to release histamine by FMLP. Cytoplasmic vesicles and granules of human basophils so stimulated for 20 s were gold-labeled, indicating the presence of histamine. Cytoplasmic vesicles may play a key role in the secretion of histamine from basophils in those diseases characterized by the ultrastructural morphology of piecemeal degranulation.

Basophils↗

PubMed1996

Signal transduction by IgG receptors induces calcium mobilization, but not histamine release, in the human basophilic cell line KU812F.

Human blood basophils selectively express Fc gamma RII (CDw32) among IgG receptor subtypes, but its functional role in allergic reactions remains unknown. Using the human basophilic leukemia cell line KU812F as a model system, we investigated cellular signaling events mediated through IgG receptor stimulation. KU812F cells express Fc gamma RII on their surface. mRNAs for both Fc gamma RIIA and IIB subtypes were detected by reverse transcriptase-PCR analysis. In this cell line, Fc gamma RII stimulation induced mobilization of free intracellular calcium and actin polymerization. Yet, no significant histamine release was observed, nor did blood basophils stimulated by anti-Fc gamma RII monoclonal antibody IV.3 and by a secondary antibody release histamine. These data indicate that Fc gamma RII stimulation induces cellular signaling events such as calcium mobilization in human basophils. However, these events do not lead to histamine release.

Actins↗

PubMed1996

Cytokine priming of human basophils: description of allergen 'nonreleasers'.

Interleukins 3 and 5 and GM-CSF enhance histamine release from basophils triggered by various stimuli. In this report, we describe a subset of allergic patients whose basophils release histamine in response to allergen only when primed with cytokine. In the absence of cytokine, there is no detectable response to allergen. These patients, who represent 4-13% of the allergic population, cannot be distinguished by skin test reactivity or severity of allergic symptoms. Allergen nonreleasers tend to have lower titers of allergen-specific IgE than the majority of atopic subjects, but this difference is not significant (average titer of 29.8 for nonreleasers vs. 188 for typical allergies; p = 0.15). They release histamine normally with anti-IgE and with fMLP, indicating that basophils are responsive to signalling through the IgE receptor, and there is no intrinsic defect in degranulation. Thus, in these patients, the IgE-mediated release of inflammatory mediators from basophils is dependent on, rather than merely enhanced by, T cell cytokines. The relationship between these patients and the previously described anti-IgE 'nonreleasers' is discussed.

Antibodies, Anti-Idiotypic↗

PubMed1997

Vesicular transport of Charcot-Leyden crystal protein in f-Met peptide-stimulated human basophils.

The ultrastructural localization of Charcot-Leyden crystal (CLC) protein during f-Met-peptide-induced degranulation of human basophils was analyzed at multiple times after stimulation. In this secretion model, piecemeal and anaphylactic degranulation occurred sequentially in stimulated cells and were followed by reconstitution of granule contents. This analysis showed that granule number and alteration and location of gold-labeled, formed CLCs changed over time. CLCs were extruded from granules and remained attached to plasma membranes early after stimulation. At later times, similar structures reappeared in granules in quantity. Smooth-membrane-bound vesicles, analyzed by number, by visible particle contents (or lack of contents) and by gold labeling for CLC protein, showed that empty vesicles increased at the earliest time sampled (0 time) and plunged thereafter in actively extruding and completely degranulated cells. Vesicles containing granule particles were elevated initially at 10 s and at later times. Gold-labeled CLC-protein-containing vesicles were of either empty or particle-filled varieties, and both types were involved with CLC protein transport out of cells at early times and into cells at later times as basophils recovered. Thus, vesicle transport of CLC protein is a mechanism for producing piecemeal degranulation and endocytotic recovery of released CLC protein from human basophils. This vesicular shuttle may be an effector mechanism for widespread piecemeal losses from granules in basophils in inflammatory sites in vivo in human disease.

Anaphylaxis↗

PubMed1985

Human lung macrophages induce histamine release from basophils and mast cells.

Human lung macrophages isolated from surgical specimens, when cultured for 24 h, acquired the capacity to induce histamine release from human basophils. This releasing activity was entirely accounted for by soluble, nondialyzable factor(s) (molecular weight, more than 2,000 daltons) released from cultured macrophages. The basophil release reaction was dose-dependent, and also Ca++ (optimal concentration = 5 mM) and temperature (optimal = 37 degrees C) dependent. Supernatants derived from the equivalent of 3 X 10(6) macrophages/ml released 50% histamine from basophils of sensitive donors. The supernatants also induced histamine release from lung mast cells. These results are the first report of a human macrophage-derived product that activates basophils and mast cells to release histamine.

Basophils↗