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At least 1,243 records · Page 69Linked to original sources
PubMed1982

Platelet satellitism to basophils in a patient with chronic myelocytic leukaemia.

Platelet satellitism to basophil granulocytes was observed in a patient with chronic myelocytic leukaemia. This phenomenon occurred with peripheral basophil cells obtained from venous blood anticoagulated with EDTA. Previous reports have demonstrated platelet satellitism to polymorphonuclear neutrophils and monocytes but not to other types of white blood cells. The cause of the platelet satellitism in this CML case remains unclear. It is suggested that this rare phenomenon should be considered in evaluating the platelet number in CML.

Aged↗
PubMed1996

Effect of interleukin-1 receptor antagonist (IL-1RA) on histamine and serotonin release by rat basophilic leukemia cells (RBL-2H3) and peritoneal mast cells.

Recently, it has been appreciated that cultured mast cells are significant sources of cytokines. However, the role of interkeukin-1 (IL-1) on mast cells and/or basophil degranulation is still unclear. In this report we provide evidence that rat basophilic leukemia cells (RBLC) cultured with a natural inhibitor of IL-1, interleukin-1 receptor antagonist (IL-1RA) (500 ng/ml) for 48 h, strongly inhibited the spontaneous release of serotonin (5HT) and histamine (from 22.50 to 43.49%), compared to untreated cells (control). When IL-1RA-treated and untreated RBLC were stimulated with a secretagogue (anti-IgE), no difference was found in the percent of 5HT and histamine release. Moreover, in another set of experiments using rat peritoneal mast cells (RPMC) treated and untreated with IL-1RA, we found that IL-1RA did not affect the release of 5HT or histamine, even when the secretagogue anti-IgE or compound 48/80 (C48/80) were used. The present studies describe an additional biological activity of IL-1RA, inhibiting histamine and 5HT release from RBLC cultures.

Animals↗
PubMed1989

Release of elastase from purified human lung mast cells and basophils. Identification as a Hageman factor cleaving enzyme.

Elastase, a serine protease, is capable of inducing severe lung destruction in experimental animal models. We now report that this proteinase exists preformed in neutrophil-free sonicates of purified human lung mast cells (greater than 98% purity) and in circulating peripheral blood basophils (greater than 97% purity). The elastase levels in both cell types (41-174 ng/10(6) cells) represents approximately 3-20% of those found in human neutrophils; both cell types released their elastase following anti-IgE and ionophore A23187 challenge. The apparent molecular size of the mast cell enzyme on Sephadex G-100 gel filtration, as well as its inhibition profile, was identical to that of purified human neutrophil elastase. This mast cell elastase is identical to our previously reported mast cell-derived Hageman factor cleaving activity. Mast cell-, basophil-, and neutrophil-derived elastases cleave Hageman factor into fragments of 52,000 and 28,000 Da; cleavage by all three enzymes is inhibited by preincubation with polyclonal antibodies directed against human neutrophil elastase.

Autoradiography↗
PubMed1991

Two-compartment basophil cell trafficking model for methylprednisolone pharmacodynamics.

A two-compartment closed model was used to characterize the movement of basophils between blood and extravascular sites resulting from methylprednisolone (MP) exposure. This model is consistent with the view that corticosteroids cause a decrease in the recirculation of these cells from peripheral compartments. Methylprednisolone (Solu-Medrol) was given to healthy males at doses of 10, 25, and 40 mg. Blood samples were collected and assayed for MP by HPLC for pharmacokinetic analysis. Whole blood histamine, an index of circulating basophils, was assessed by RIA over 32 hr. Nonlinear least-squares analysis was carried out to solve for the model parameters reflecting cell movement between compartments and sensitivity (IC50) to the steroid. This model quantitiates the fall and return pattern of biologic response to corticosteroids with a minimal number of parameters which jointly fit several dose/response curves and yields a mean IC50 value of 8.1 ng/ml similar to receptor binding of MP. Properties of the temporal and integrated response curve and model extrapolations over a wide dose range were explored with simulations. Because corticosteroids exert similar effects on other cells in blood, this model may be applicable to various regulatory and immunosuppressive effects.

Adrenal Cortex Hormones↗
PubMed1978

Basophilic leukemia presenting as gastroduodenal ulceration: effect of H-2-receptor blockade.

A patient with multiple gastroduodenal ulcers and gastric hypersecretion due to histamine excess associated with basophilic leukemia is described. Treatment with the histamine H-2-receptor blocker, cimetidine, was able to abolish the gastric hypersecretion and gastrointestinal blood loss. A literature review produced four other cases of multiple gastroduodenal ulceration with this disease, suggesting that it is more common than previously recognized. The availability of a potent H-2-receptor antagonist offers effective and specifically tailored therapy to counteract the gastrointestinal effects of hyperhistaminemia in basophilic leukemia and other "histamine excess" diseases.

Adult↗
PubMed1987

Human basophil degranulation test in liver hydatidosis.

Upon exposure to a specific antigen, granulation of basophils bearing IgE disappears. The aim of this study was to assess the human basophil degranulation (HBD) test with hydatic antigen in 100 patients. Seventy patients were clinically suspected of having liver hydatidosis (LH) (group I). Eight patients had asymptomatic hepatic calcifications. Twenty-two patients had previous surgery for LH (group III). In group I the percentage of HBD was significantly higher in patients with LH (23 of 70) than in patients with other hepatobiliary diseases (P less than 0.001). In group II all patients had negative HBD tests. In group III the test became negative within 8-12 months after radical surgery in four patients, and remained positive in the other 18. These results suggest that the HBD test is useful for the diagnosis of LH. In asymptomatic patients with hepatic calcified cyst, a negative HBD test suggests a dead parasite. In previously operated patients, a positive test suggests persistence of antigen.

Animals↗
PubMed1982

[Histamine concentration in the arterial and venous blood, plasma and basophile leucocytes on patients with chronic obstructive bronchitis and on healthy persons ].

Patients with chronic obstructive bronchitis (non atopics) show significant increased histamine concentrations in the plasma. In these patients the histamine concentration in the whole blood was also higher. The histamine concentration in the blood reflect primarily the concentration of basophiles. In individual patients very high plasma and whole blood histamine concentrations were found. The concentration of histamine in the venous plasma was about 2/3 of this of the arterial plasma. No difference in basophile histamine concentration was observed between patients and controls. The histamine concentrations in the plasma reflect primarily the high local histamine concentration in the bronchial mucosa. The plasma histamine concentration itself does not act as direct bronchoconstrictor. The histamine dependent bronchoconstriction is believed to be mostly reflex bronchoconstriction by challenge locally the sensoric receptors in the bronchial mucosa.

Basophils↗
PubMed1985

Cell instability in basophil leukocytes of patients with chronic obstructive airway disease.

The histamine release from basophils induced by hypo-osmolarity was investigated in 75 healthy persons and in 43 patients with chronic obstructive airway disease. Leukocyte suspensions were diluted with destilled water in cell/water ratio volumen of 1:1, 1:3, and 1:7. Basophils, sequentially treated with increasing amounts of water, show an activation of the release process. A statistically significant age-dependent hypo-osmolar histamine liberation could be demonstrated. Furthermore, a significant higher cell stability was found for the group of patients.

Adult↗
PubMed1992

Mechanical agitation of very dilute antiserum against IgE has no effect on basophil staining properties.

A previously reported effect of mechanically agitated dilutions of antiserum raised against IgE was investigated using the loss of metachromatic staining properties of human basophil leukocytes as a model. A series of 24 blind experiments was performed in which we determined the number of toluidine blue-stainable basophils after incubating with vortexed or non-vortexed dilutions of anti-IgE. Tenfold serial dilutions were used, in the range 10(21) to 10(30) (6.6 x 10(-26) to 6.6 x 10(-35) M anti-IgE). We found no evidence for a different effect of strongly agitated dilutions, compared to dilutions made with minimal physical agitation. In fact, in our hands no effect of extreme dilutions was shown at all. We conclude that the effect of extreme dilutions of anti-IgE, reported by Davenas et al., needs further clarification and that in this process the reproducibility of results between experimenters should be carefully determined.

Basophils↗
PubMed1993

Histamine release from basophils in childhood: age dependency and inhibition by pertussis infection and pertussis toxin.

The influence of childhood pertussis infection and of purified pertussis toxin on histamine release from human basophil leucocytes was investigated. Three different stimuli, the peptide N-formyl-Met-Phe (NFMP), anti-IgE, and the calciumionophore A23187 were used to challenge the cells. When NFMP was the stimulus, histamine release in the control group (age 0.5-17 years) increased in an age-dependent fashion, whereas anti-IgE and A23187 stimulated release did not vary with age. During the convulsive state of pertussis infection there was a significant reduction of histamine release in response to 10 microM NFMP (from 9.5 +/- 1.4 [n = 21] to 6.7 +/- 1.5 [n = 19], P < 0.05) and in response to 800 and 80 U/ml anti-IgE (from 28.5 +/- 5 [n = 19] to 16.3 +/- 5 [n = 13], P < 0.05, and from 6.9 +/- 1.7 [n = 16] to 2 +/- 0.8 [n = 13], P < 0.01), whereas histamine release stimulated by A23187 was unchanged compared to release in control children. In vitro pretreatment of basophils from healthy children and adults with pertussis toxin also inhibited histamine release. When NFMP was the stimulus, release was completely blocked by pertussis toxin with an IC50 of about 11 ng/ml, whereas anti-IgE stimulated release was only inhibited by 20%-30% and release induced by A23187 was reduced to 40%-50% by toxin treatment. In conclusion we have demonstrated a functional impairment of histamine release during the convulsive state of pertussis and that this inhibition is likely to be mediated by pertussis toxin.

Adolescent↗
PubMed1986

Functional differences between human cutaneous mast cells and basophils: a comparison of morphine-induced histamine release.

Intravenous administration of morphine sulfate often produces urticarial and hypotensive reactions associated with elevations in plasma histamine. The source of this histamine and mechanisms controlling its release are poorly understood. Previous studies of morphine-induced histamine release compared human leukocytes to rat peritoneal mast cells. The effects of morphine on human cutaneous mast cells has not been examined. We studied in vitro histamine release from human basophils and human skin preparations containing cutaneous mast cells to evaluate their relative contribution to the pharmacologic effects of morphine. Human skin mast cell preparations showed dose-dependent histamine release over a morphine concentration range of 1.5 X 10(-5) to 4.5 X 10(-3) M, with peak release occurring at 5 X 10(-4) M, with peak release occurring at 5 X 10(-4) M. Clinically, morphine sulfate is usually injected as a 1.5 X 10(-2) M solution. Histamine release was calcium dependent and equivalent to that obtained with 3 and 10 mM strontium. Morphologic examination revealed degranulation and exocytosis occurring in morphine-stimulated tissue but not in specimens exposed to buffer alone. Lactate dehydrogenase levels did not increase following morphine incubation, thus supporting a noncytolytic mechanism of histamine release. Basophils, in contrast, showed no significant histamine release from exposure to morphine up to 10(-2) M. Concanavalin A, as a positive control in these same preparations, produced a mean histamine release of 21.0%.(ABSTRACT TRUNCATED AT 250 WORDS)

Basophils↗
PubMed1986

Interaction of monoclonal antibodies with the IgE-receptor on rat mast cells and rat basophilic leukemia (RBL) cells.

The close relation between rat mast cells and rat basophilic leukemia (RBL) cells with regard to the presence of receptors for IgE and Fc gamma led us to generate monoclonal antibodies directed against cell surface antigens. Hybridomas were obtained by the fusion of NS1 mouse myeloma cells with murine spleen and lymph node cells. The culture supernatants were assayed by two ELISA techniques: a) for the production of mouse immunoglobulin in general and b) for antibodies directed against surface antigens of RBL cells. For this purpose RBL cells were attached to polyvinyl chloride microtitre plates. Eight hybrids produced antibodies directed against surface antigens on RBL cells. Hybrids were cloned and characterized with regard to their isotype and light chains. All eight clones secreted IgM with K light chains. Immunofluorescence studies performed with RBL cells revealed that all eight antibodies were able to show a specific fluorescence. Furthermore, four of these eight antibodies also showed a specific fluorescence with purified rat mast cells. These four antibodies were analyzed as to their ability of interacting with the IgE-receptor on RBL cells and purified rat mast cells. They reduced the binding rate of radiolabelled rat IgE to RBL and rat mast cells. A mutual inhibition of the passive cutaneous anaphylaxis (PCA) reaction in the rat by either mixing mouse reaginic serum directed against 2,4-dinitrophenol bovine serum albumin (DNP-BSA) or by mixing monoclonal mouse anti-DNP IgE with the monoclonal mouse anti-cell surface (rat basophilic leukemia, rat mast cell) IgM was determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Histamine releasing lymphokine: preliminary evidence of membrane receptors on basophils.

Histamine release induced by the lymphokine-histamine releasing factor (HRF), like IgE-mediated release is a two step event--the Ca2+-independent activation step in which HRF primes the cells for histamine release and the Ca2+-dependent histamine release. The stimulus produced by the activation step decays relatively slowly and exponentially with a half-time of 38 min. By the 'receptor desensitization' approach, HRF appears to possess specific receptors on basophils as demonstrated by its ability to desensitize the cells to itself for subsequent histamine release. Cross desensitization experiments further suggested that a close relationship might exist between any such receptors and cell-bound IgE molecules, since desensitization of cells to anti-IgE also resulted in their desensitization to HRF as well; though the reverse was not the case. Nevertheless, any such relationship does not involve binding and cross linking of cell-bound IgE molecules by HRF. The putative HRF receptors may be distinct from those proposed for macrophage migration inhibitory factor (MIF) and leucocyte migration inhibitory factor (LIF) since, unlike the latter lymphokines whose interactions with their target cells show specificity for certain simple sugars, HRF's interaction with basophils show no such specificity to any of the simple sugars tested.

Acetylglucosamine↗
PubMed1983

A study of histamine release from human basophils and lung mast cells by products of lymphocyte stimulation.

It has been previously reported by Thueson and his co-workers [1] that lymphokine-containing supernatant of cultured human peripheral blood lymphocytes stimulated with Concanavalin-A (Con-A) is capable of releasing histamine from human basophils. Here we confirm such findings, show that such release is additive to that due to immunological stimuli (Anti-IgE and antigen) and describe its characteristics and effect in lung tissue. The lymphokine was found to induce a small histamine release from chopped or enzyme-dispersed human lung tissue. As was the case with basophils, the release from lung tissue by this factor, though small, was also found to be additive to that induced by anti-IgE when both agents were added simultaneously. Histamine release from leucocytes by neat supernatant ranged from 9 to 35% and up to 55% when concentrated four-fold. The release resembled that of IgE-mediated reactions in many respects including temperature and calcium dependence, time course and susceptibility to metabolic inhibitors - thus suggesting a non-cytotoxic mechanism. These results show that histamine release by this lymphokine(s) possesses most of the features of an active secretory process. They also suggest that the histamine-releasing factor (HRF) in lymphokine-containing supernatants might be involved in the modulation of type I allergy in humans, apart from its involvement in delayed-type hypersensitivity.

Antigens↗
PubMed1987

Complexity of the influence of gangliosides on histamine release from human basophils and rat mast cells.

The influence of exogenous addition of gangliosides on histamine release from human basophils and rat mast cells was examined in vitro. Gangliosides dose-dependently inhibited histamine release, and this inhibition was dependent on the ganglioside sialic acid content, since GT1b, having 3 sialic acid moieties, was more potent than gangliosides with 2 moieties (GD1a and GD1b), which again were more potent inhibitors than GM1 with one moiety. Asialo-GM1 was without effect. In high concentrations the gangliosides potentiated basophil histamine release. The modulation of histamine release was reflected in the sensitivity of the cells to extracellular calcium, since inhibition of the release could be counteracted by increasing the extracellular concentration of calcium.

Animals↗
PubMed1993

Pharmacological investigations with different protein kinase C inhibitors on IgE-dependent and IgE-independent activation of human basophils.

In the present study different selective inhibitors of the multifunctional serine/threonine kinase protein kinase C (PKC) were investigated on classical activation pathways of basophils in comparison to the nonselective protein kinase inhibitor staurosporine. The potent inhibitors Ro 31-7549, Ro 31-8220, calphostin C and ilmofosine (BM 41.440), which show selectivity for PKC in vitro, significantly potentiated Fc epsilon RI-mediated histamine release up to 50% vs. controls at concentrations > 10(-7) mumol/l but were without any intrinsic histamine releasing activity. Direct activation of cellular PKC by phorbol ester was suppressed by all compounds apart from ilmofosine at the same concentrations. We did not observe statistically significant effects of selective PKC inhibitors on exocytosis induced by the peptide formylmeth-leu-phe (FMLP) or the ionophore A23187, whereas staurosporine potentiated the FMLP-induced histamine release in a dose-dependent fashion: maximum potentiation was 63.5 +/- 8.9% vs. control at 1 mumol/l (n = 4). The findings suggest that PKC exhibits differential functions during biochemical events of stimulus-secretion coupling in human basophils supposedly by its distinct subtypes. With respect to the present data, TPA-induced and IgE-mediated signals are not closely correlated.

Alkaloids↗
PubMed1985

Histamine release from human basophils by pepstatin A.

Pepstatin A, a pentapeptide isolated from cultures of actinomycetes, induced histamine secretion from human basophils in the concentration range of 3 X 10(-7) to 10(-4) M. The characteristics of this reaction were similar to those of f-met-peptide-induced histamine release: pepstatin A-induced release required Ca2+ and the release reaction was complete within 2 min at 22 or 37 degrees C, but did not occur at 4 degrees C. Release by both pepstatin A and f-met-peptide was reversibly inhibited by two non-releasing analogs of f-met-peptide, CBZ-Phe-Met and BOC-Met-Leu-Phe. Further, there was complete cross-desensitization between pepstatin A and f-met-peptide, while cells desensitized to pepstatin A released normally with anti-IgE and vice versa. A variety of pharmacological agents had similar effects on both pepstatin A and f-met-peptide-induced release (e.g., no enhancement with D2O; marked enhancement with cytochalasin B). We suggest that pepstatin A induces histamine release from human basophils by activating a cell surface receptor(s), also activated by the synthetic tripeptide f-met-peptide.

Basophils↗
PubMed1992

Ionic regulation of human basophil releasability. I. Inhibitory effect of copper.

The effects of copper (CuSO4 and CuCl2) on in vitro histamine release from human basophils stimulated by anti-IgE and Ca2+ ionophore A23187 were evaluated. Both CuSO4 and CuCl2 caused a dose-related inhibition of histamine release, which was more pronounced on anti-IgE- than on Ca2+ ionophore-induced histamine release. The concentration which produced 50% inhibition of anti-IgE-induced histamine release was 1.3 microM for CuSO4 and 1.5 microM for CuCl2; the maximal inhibition of Ca2+ ionophore-induced histamine release was 33% for CuCl2 (4 microM) and 51% for CuSO4 (16 microM). The inhibitory effect on anti-IgE-induced histamine release persisted also when extracellular Cu2+ was removed by cell washing before stimulation, whereas no inhibition of Ca2+ ionophore-induced histamine release was found when extracellular Cu2+ was removed. The activity of Cu2+ was independent of any effects of deuterium oxide and colchicine, two agents known to interact with microtubules. Increased extracellular Ca2+ concentrations reduced the inhibitory effect of CuCl2 on Ca2+ ionophore-induced histamine release, and Schild plot analysis demonstrated that Cu2+ ions are competitive antagonists of Ca2+ ions. These results indicate that Cu2+ ions in the micromolar range down-regulate anti-IgE- and Ca2+ ionophore-induced histamine release. Since Cu2+ concentration in human plasma is in the micromolar range (30 microM with 10-30% of free Cu2+), it is conceivable that Cu2+ ions contribute to the in vivo regulation of histamine release from human basophils.

Adult↗