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At least 973 records · Page 54Linked to original sources
PubMed1984

Acute basophilic leukemia.

Acute basophilic leukemia was diagnosed in a 61-year-old black woman on the basis of 85 to 90 percent basophils in the peripheral blood as well as bone marrow and very high serum histamine level (more than 10,000 ng/ml). These complications occurred as a transformation from essential thrombocythemia. Accompanying this transformation, there was also cytogenetic change from 46XX karyotype to 46XX 2p+ in 66 to 90 percent of cells in the bone marrow. This may be the first reported occurrence of transformation of essential thrombocythemia into acute basophilic leukemia.

Acute Disease↗
PubMed1981

Secretion from rat basophilic leukaemia cells induced by calcium ionophores. Effect of pH and metabolic inhibition.

Previous experiments on the functional properties of rat basophilic leukaemia cells showed a major anomaly when compared to normal mast cells: though IgE-mediated secretion was dependent on external Ca2+ with both types of cells, substantial non-cytotoxic release with ionophore A23187 could be demonstrated with the normal cells but not with the tumour cells. We now show that when the pH of the incubation medium is increased to 8 it is possible to obtain excellent Ca-dependent, non-cytotoxic secretion from tumour basophils with the ionophores A23187 and ionomycin. These results provide further evidence that secretion from the tumour cells occurs via a mechanism similar to that used by normal mast cells and basophils. Experiments with metabolically inhibited tumour cells suggest that their unusual sensitivity to the cytotoxic effects of Ca2+ ionophores may be related to their ability to sequester intracellular calcium. Changes in the conditions of cell culture appeared to produce substantial and at least partially reversible changes in responsiveness to IgE-mediated triggering and ionophores.

Animals↗
PubMed1996

Receptor-independent G protein activation may account for the stimulatory effects of first-generation H1-receptor antagonists in HL-60 cells, basophils, and mast cells.

The first-generation histamine H1-receptor antagonists, chlorpheniramine (CPHE) and diphenhydramine (DPH), may activate histamine release from basophils and mast cells. Because CPHE and DPH are cationic-amphiphilic and because several substances with such physicochemical properties activate heterotrimeric regulatory guanine nucleotide-binding proteins (G-proteins) in a receptor-independent manner, we asked the question of whether or not H1-receptor antagonists could be G-protein activators as well. In dibutyryl cAMP-differentiated HL-60 cells, CPHE and DPH increased cytosolic Ca2+ concentration and azurophilic granule release in pertussis toxin (PTX)-sensitive manners. In HL-60 membranes, PTX-sensitive stimulations of GTPase [E.C. 3.6.1.] and binding of guanosine 5'-[gamma-thio]triphosphate by H1 receptor antagonists were observed. CPHE and DPH also increased GTP hydrolysis by the purified PTX-sensitive G-protein, transducin. In all-trans-retinoic acid-differentiated HL-60 cells and rat basophilic leukemia cells (RBL 2H3 cells), H1-receptor antagonists induced, unlike in dibutyryl cAMP-differentiated HL-60 cells, Ca2+ influx without Ca2+ mobilization from intracellular stores. CPHE and DPH also induced serotonin release from RBL 2H3 cells. Our data indicate that first-generation H1-receptor antagonists are receptor-independent G-protein activators and that such a mechanism of action accounts for their stimulatory effects in HL-60 cells, basophils, and mast cells.

Animals↗
PubMed1984

Ixodes holocyclus: kinetics of cutaneous basophil responses in naive, and actively and passively sensitized guinea pigs.

In guinea pigs, macroscopic cutaneous reactions to initial (primary) Ixodes holocyclus feeding were first apparent at 96 hr post-tick attachment, peaked at 7 days (5 mm), and were gone by Day 14. Microscopic analyses of these primary tick feeding sites at 12, 24, 48, 72, and 96 hr post-attachment revealed the dominance mononuclear cells (63-94% of the infiltrate) at all times. Neutrophil levels were high initially (34% of the infiltrate), but quickly subsided to 6-15% of the cellular response. Eosinophils were essentially absent from primary sites, comprising only 1-3% of the infiltrate. Basophils were absent initially, but accumulated in small but significant numbers (12% of the infiltrate) at the epidermal-dermal border by 96 hr post-tick attachment, 3 days prior to maximum erythematous skin reactions. In sensitized and challenged (secondary) animals, erythematous reactions in response to secondary tick feeding were apparent as early as 18 hr post-tick attachment with peak responses at 48 hr (3-4 mm). Cutaneous leukocyte responses to challenge feedings were quantitated at 12, 24, 48, and 72 hr post-tick attachment and consisted initially (12-24 hr) of a strong mononuclear cell response (72-79% of the infiltrate) that was replaced by a dominant basophil response at 48 and 72 hr. Strong cutaneous basophil responses coincided with a significant level of tick rejection. Eosinophils and neutrophils were virtually absent from these secondary responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Inflammatory component of celiac sprue mucosa. I. Mast cells, basophils, and eosinophils.

To study mast cell, basophil, and eosinophil populations within celiac sprue mucosae in comparison with various disease-control specimens, toluidine blue-stained 1-micron plastic sections were analyzed morphometrically by light microscopy. Within lamina propria of celiac sprue mucosae each population of cells was markedly expanded and fell to control levels during gluten restriction. Changes within surface and crypt epithelium, however, were not significantly different from those in the severer, "flat" disease-control lesions, and were not affected by gluten restriction. Basophils were not identified within surface or crypt epithelium of any specimen analyzed. The influx of eosinophils and basophils into lamina propria occurred by emigration via pericryptal venules. Mature mast cells were not seen within the microvasculature, neither were these cells undergoing mitosis: thus their origin was from unidentified precursors. The gluten-dependent alterations in each of these cell populations in celiac sprue mucosae are consistent with secondary effector mechanisms, probably resulting from cell-mediated reactions that occur primarily within the lamina propria, rather than the epithelium.

Basophils↗
PubMed1983

A single centrifugation step method for the simultaneous separation of different leukocytes with special reference to basophilic leukocytes.

A simple method of separating mononuclear leukocytes, basophils, neutrophils and an eosinophil fraction from human blood is described, using discontinuous Percoll gradient centrifugation. Mononuclear cells were found in the upper layer (band 1) at a density of less than or equal to 1.072. The second band with a density of less than or equal to 1.082 contained most of the basophilic leukocytes (av. 70% and 8-20% of the differential cell count) and a minor part of the mononuclear cells (av. 8%). In the third band, density less than or equal to 1.1, 82-91% of the polymorphonuclear cells (PMN) were found, consisting mainly of neutrophils. 35-70% of the eosinophilic PMN cells are located in band four (density greater than 1.1). The function of the basophil-enriched fraction was tested by degranulation with specific antigen.

Basophils↗
PubMed1986

Single step enrichment of human peripheral blood basophils by Ficoll-Paque centrifugation.

A simple, rapid and economical method for the enrichment of basophils from peripheral blood with high recovery is described. Peripheral blood was layered over a Ficoll-Paque cushion and centrifuged. The Ficoll-Paque layer was aspirated taking care not to disturb the interphase and the buffy coat. The Ficoll-Paque layer contained most of the basophils. A recovery of 82% (65-95%) and a 23.5-fold enrichment of basophils with their morphology and biological activity preserved was achieved.

Antibodies, Anti-Idiotypic↗
PubMed1987

Immunogold probe for the light-microscopic phenotyping of human mast cells and basophils.

A method is presented whereby light microscopic phenotyping of human basophils and lung mast cells was obtained by simultaneous labeling of surface antigens with specific mouse monoclonal antibodies and an anti-mouse IgG immunogold probe and histochemical staining with alcian blue, a highly specific stain for these cells' granules. The double labeling technique offers a useful immunohistochemical method for the phenotyping of basophils and mast cells in impure cell preparations. The procedure is relatively simple and requires small cell samples while providing accurate information on functional and differentiation markers. Preliminary results of human lung mast cell and peripheral blood basophil phenotyping discloses class I histocompatibility antigens on both cell types and class II antigen HLA DR on 10-20% of mast cells alone. Lung mast cells also unexpectedly exhibit the leukocyte marker HLE-1.

Antibodies, Monoclonal↗
PubMed1993

Purification of human blood basophils by negative selection using immunomagnetic beads.

A simple and rapid method for isolating highly purified and functionally intact basophils from normal human blood is described. Blood from healthy volunteers was centrifuged through a two layer Percoll density gradient. The majority of the basophils were recovered between Percoll layers with densities of 1.070 and 1.080, constituting 45.6% of total leukocytes. Lymphocytes, monocytes and neutrophils were extracted from this fraction using a panel of mabs in a direct or indirect selection procedure using immunomagnetic beads (Dynabeads) coated with sheep anti-mouse IgG. These negative immunoselection procedures produced a high yield of basophils with a mean purity of 97.8% (range 93.0-99.5%) and 97.0% (range 96.2-99.0%) using the direct and indirect method, respectively. The cells isolated by this method are viable, release histamine to various stimuli in a normal manner, and appear morphologically normal in transmission electron microscopy.

Basophils↗
PubMed1980

Existence of basophil chemotaxis in subjects with hay fever.

From an earlier study we proposed that the relative peripheral basophilia of subjects with symptomatic hay fever might be associated with a basophil chemotactic factor in the serum. Six subjects with symptomatic hay fever and six nonallergic subjects were tested for basophil chemotaxis (BC) weekly during and after the hay fever season. Cells of the allergic subjects with autologous serum showed significantly more BC than with control serum during the symptomatic weeks. After they hay fever season there was no difference in BC between the allergic and nonallergic groups. We conclude that there is a BC factor(s) in the serum of symptomatic subjects with hay fever which requires basophils from symptomatic subjects to be demonstrable.

Basophils↗
PubMed1985

Role of human basophils and mast cells in the pathogenesis of allergic diseases.

The role of human basophils and mast cells in the pathogenesis of allergic diseases has been analyzed. Purified human basophils and mast cells release several known mediators of allergic reactions, including histamine, sulfidopeptide leukotrienes, kinin-forming enzymes, and, in the case of the mast cell, PGD2. These same mediators are released in vivo after experimental challenge in the upper airways with either allergen or cold, dry air, a stimulus used to simulate exercise-induced bronchospasm. The appearance of mast cell mediators in vivo after such challenges further implicates mast cells in the pathogenesis of allergic diseases of the airways that occur as a result of exposure to allergen or physical stimuli. During the LPR after experimental challenge of the upper airways, the pattern of mediators released (i.e., histamine, leukotrienes, and others, but no PGD2) suggests that basophils may contribute to the LPR. Antiallergic drugs that prevent mediator release in vitro, such as antihistamines, also prevent the appearance of mediators in vivo, strengthening both the validity of the in vitro test as a model of the disease and the hypothesis that mediator release is an essential element of the disease process. A model discussing the pathogenetic mechanism is presented.

Adrenal Cortex Hormones↗
PubMed1986

Characteristics of diatrizoate-induced basophil histamine release.

Factors influencing the release of histamine by basophils exposed to the radiocontrast agent diatrizoate were investigated in vitro by use of cells from healthy adult subjects with no history of radiocontrast reactions. Diatrizoate-induced release shared similarities with calcium ionophore-induced release. The response to both agents is dose dependent, enhanced by deuterium oxide, optimal at 37 degrees C, calcium dependent, and enhanced with longer reaction times. Unlike calcium ionophore, however, pretreatment of basophils with diatrizoate may also induce dose-dependent inhibition of reactivity during subsequent challenges with anti-IgE, N-formyl methionine peptide, and calcium ionophore. These findings suggest that diatrizoate may induce histamine release via a calcium ionophore-like mechanism, but other effects on cellular function probably account for its ability to inhibit basophil responsiveness.

Anaphylaxis↗
PubMed1989

Azelastine inhibits IgE-mediated human basophil histamine release.

To examine the mechanism potentially contributing to therapeutic efficacy of azelastine in allergic rhinitis and asthma, we studied the effect of azelastine on stimulated histamine release from basophils prepared as a mixed leukocyte suspension from human blood. Azelastine was found to significantly inhibit anti-IgE-stimulated basophil histamine release. Time-course experiments indicated that the inhibitory effect of azelastine was immediate and that preincubation of basophils in azelastine was not necessary. In dose-response experiments with azelastine, 1 to 100 mumol/L, significant inhibition of histamine release was consistently observed in azelastine concentrations greater than or equal to 10 mumol/L. This inhibition was dose dependent (r = 0.96; p less than 0.001) with maximal mean inhibition of 91 +/- 8% at 100 mumol/L of azelastine.

Basophils↗
PubMed1992

Role of sodium in mediator release from human basophils.

We studied the effect of extracellular sodium concentration on histamine release (HR) from human basophils initiated by immunologic and nonimmunologic stimuli. We found that lowering extracellular sodium markedly enhances HR induced by an immunologic stimulus from these cells. In buffer in which sodium had been replaced with univalent ions of strong bases, enhancement of HR increased as extracellular sodium decreased. Enhancement was the result of increased duration of release. When sucrose was used for replacement of sodium, we also observed that enhancement of HR increased as extracellular sodium decreased, but there was some lessening of enhancement at [Na+]e between 5 and 10 mmol/L. Ouabain, which is an inhibitor of the Na+/K+ adenosine triphosphatase, and bumetanide and furosemide, which are inhibitors of Cl(-)-dependent Na(+)-K+ cotransport, caused small increases in enhancement of HR by sodium-deficient buffers; 4,4'-diisothiocyanostilbene-2-2'-disulfonic acid, an anion transport inhibitor, caused some inhibition of enhancement of HR. Analogues of amiloride, such as 5-(N-N-hexamethylene) amiloride (HMA) and 5-(N-4-chlorobenzyl)-2'-4'dimethylbenzamil (CBDMB), inhibit Na+/H+ exchange, Na+/Ca++ exchange, and Na+ channels. Interestingly, at higher doses, HMA and CBDMB caused marked enhancement of HR in both normal and sodium-deficient buffers. These results suggest that several cellular regulatory mechanisms potentially are important for normal basophil secretion. The most likely are pH regulatory mechanisms that include Na+/H+ exchange and anion exchangers that transport alkaline equivalents. Our findings enhancement of basophil HR by HMA and CBDMB is particularly noteworthy in light of the recent interest in use of amiloride by inhalation for therapy of lung disease in patients with cystic fibrosis.

Basophils↗
PubMed1993

Induction of specific histamine release from basophils with purified natural and recombinant birch pollen allergens.

As much as 15% of the population in industrialized countries suffers from type I allergic symptoms (rhinitis, conjunctivitis, and bronchial asthma). One approach toward this disease involves the production of recombinant allergens in Escherichia coli and their purification for diagnostic and therapeutic purposes. In this study we compared the IgE-binding capacity of natural and recombinant birth allergens with their functional ability to release histamine from allergic patients' basophils via cross-linking of high-affinity Fc epsilon-receptors. The recombinant as well as pollen-derived Bet v I and birch profilin (Bet v II) were purified and tested in parallel on IgE immunoblots and in in vitro histamine release tests (n = 21). We observed an excellent correlation between allergen-induced histamine release and birch pollen RAST (r = 0.881, p < 0.002). Nonspecific histamine release as a result of a cell toxic effect of the allergen preparations was never observed from basophils of donors without birch pollen allergy. The specificity of the presented effector model is also documented by the specific desensitization of patients' basophils with the recombinant allergens. These data may provide a basis for the use of purified recombinant allergens in sensitive and specific in vitro allergy tests monitoring the effector situation in allergic patients, which therefore may represent a possible alternative for in vivo diagnostic methods.

Allergens↗
PubMed1980

A model of cell activation and desensitization by surface immunoglobin: the case of histamine release from human basophils.

We present a model for the control of immunoglobulin E (IgE)-mediated histamine release from human basophils. We suggest that there is a calcium gating factor which interacts with crosslinked IgE to form a short-lived open calcium channel. After formation of the channel the activated gating factor rapidly decays to an inactive form. It is the loss of the active gating factor which causes the basophil to desensitize nonspecifically. We propose that the crosslinked IgE molecules are deactivated by a mechanism, such as endocytosis or shedding, which is independent of the mechanism which inactivates the calcium gating factor. This loss of functional IgE leads to specific desensitization. The mathematical formulation of the model explains the relationship of specific and nonspecific desensitization to the amount of specific IgE on the basophil surface; explains why there are two types of antigen excess inhibition; explains the relationship between antigen excess inhibition and desensitization; explains why, for a fixed antigen concentration, increasing the concentration of cell surface IgE increases histamine release until an optimal concentration is reached, then decreases histamine release; predicts the effects that changing the external calcium will have on the dose response curve; and predicts that increasing the amount of specific IgE on the cell surface will cause the dose response curve to undergo a transition from a curve with a single maximum to a curve with two maxima.

Basophils↗
PubMed1989

Medium pH determines the differentiation of human promyelocytic leukemia cells to basophils or eosinophils by culturing in a protein- and serum-free medium.

Cells containing large basophilic granules in the cytoplasm appeared after culturing human promyelocytic leukemia cells (HL-60) in a protein- and serum-free alkaline medium. These granules were stained with toluidine blue and alcian blue. Cells were morphologically and cytochemically similar to basophils. The existence of histamine in the cell lysates was detected in both uninduced and alkaline medium-induced HL-60 cells. After culturing HL-60 cells in a protein- and serum-free acidic medium, cells containing eosin-stained small granules (eosinophils) appeared. The differentiation of HL-60 cells to basophils or eosinophils may therefore depend on medium pH by culturing in a protein- and serum-free medium.

Basophils↗
PubMed1990

Philadelphia chromosome-negative acute hematopoietic malignancy: ultrastructural, cytochemical and immunocytochemical evidence of mast cell and basophil differentiation.

We describe a patient with fever and multiple osteolytic bone lesions accompanied by hypercalcemia, a duodenal ulcer, anemia, and thrombocytopenia. Bone marrow showed a dense infiltration by abnormal cells characterized by small basophil granula, erythrophagocytosis and nuclear atypia. These cells were positive for toluidine blue and partly for myeloperoxidase and chloroacetate esterase, expressed myeloid differentiation markers, and exhibited multiple numerical and structural chromosome aberrations. Molecular genetic analysis showed no breakpoint cluster region rearrangement. Electron microscopy demonstrated granula both of basophil and mast cell type. Concluding, in this patient an acute hematopoietic malignancy with many features of malignant mastocytosis but also with signs of a basophil differentiation. This is further support for a hematopoietic stem cell origin of human mast cells.

Adult↗