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At least 739 records · Page 41Linked to original sources
PubMed1998

Basophilic differentiation of the human leukemia cell line KU812 upon treatment with interleukin-4.

The human leukemia cell line KU812 had been described as an immature prebasophilic cell line and exhibits a potential to differentiate into mature basophils. We studied the effect of interleukin-4 (IL-4) on the basophilic differentiation of KU812 cells. When KU812 cells were cultured with 1 ng/ml IL-4, cellular histamine content increased more than 10-fold. IL-4 also enhanced the expression of Fc epsilon RI alpha, a high affinity IgE receptor, on the cell surface. KU812 cells treated with IL-4 expressed higher levels of Fc epsilon RI alpha, Fc epsilon RI beta and Fc epsilon RI gamma mRNA than non treated KU812 cells. After 21 days in culture with IL-4, KU812 cells became morphologically mature basophilic cells as demonstrated by staining positive for cytoplasmic granules and heparin proteoglycan by Wright dye and toluidin blue dye respectively. In addition, IgE-mediated histamine release was observed, suggesting that the Fc epsilon RI induced by IL-4 was functional and was able to transduce a signal for degranulation. These results suggest that IL-4 promotes differentiation of KU812 cells into mature basophilic cells both morphologically and functionally.

Basophils↗
PubMed1987

Comparison of histamine release and prostaglandin E2 production of human basophils in atopic and normal individuals.

The influence of arachidonic acid (AA) metabolism upon histamine release (HR) from human basophils after stimulation with anti-IgE was studied in 23 atopic and 11 normal individuals. HR occurred significantly faster in atopics than in normals; the total amount of HR after a 40 min incubation period was not significantly different between the two groups. Indomethacin and acetylsalicylic acid (ASA) increased the quantity of HR significantly both in atopics and normals without influencing the time course. Addition of exogenous PGE2 decreased HR; here atopics were more affected than normals 5 and 10 min after challenge with anti-IgE. Production of PGE2 after stimulation with anti-IgE was very low in both groups (in the range of 30-50 pg/10(6) cells) and often below detection limit (10-20 pg/ml). Addition of glutathione (GSH), a coenzyme of PGE2-isomerase, increased PGE2 production 2 to 5-fold during stimulation with anti-IgE. These data support the idea that arachidonic acid metabolites play an important role in modulating the "releasability" of human basophils. It is suggested that the basophils of atopic individuals may release their histamine faster than normals - perhaps on the basis of a more slowly acting endogenous feedback mechanism by PGE2. Both phenomena support the idea of an altered "releasability" of basophils from atopics compared to normals.

Adolescent↗
PubMed1979

Estimation of kinetic parameters of neutrophilic, eosinophilic, and basophilic granulocytes in human blood.

Two hematologically normal patients with glioblastoma and six patients with chronic lymphocytic leukemia received continuous 3H-thymidine infusions for 3--10 days. In autoradiographs of blood cell smears taken for 25 days or more after the beginning of 3H-thymidine administration the labeling index and the labeling intensity of granulocytes were determined. A sufficiently high labeling intensity, i.e. a sufficiently long autoradiographic exposure time was found to be critical for obtaining valid and reproducible results. On the basis of certain assumptions discussed in detail, complete labeling of cells with 3H-thymidine followed by autoradiographic evaluation and mathematical analysis of the labeling patterns seems to be a suitable method for estimation of kinetic parameters of postmitotic granulocytes in vivo. The mean intramedullary maturation and storage time was observed to be 115 +/- 7 h or neutrophils, 103 +/- 4 h for eosinophils and 103 +/- 11 h for basophils. The mean relative inflow rate into the blood (or relative turnover rate in the blood) was found to be 4.2 +/- 0.4/h for neutrophils, 4.0 +/- 0.4%/h for eosinophils and 1.2 +/- 0.3%/h for basophils. The mean blood transit time (or blood sojourn time) was estimated to be 25 +/- 2 h or neutrophils, 26 +/- 3 h for eosinophils and 89 +/- 21 h for basophils. Accordingly the half lifes (T 1/2) of granulocytes in the blood were 17.3 +/- 1.4 h for neutrophils, 18.0 +/- 2.1 for eosinophils and 62 +/- 15 h for basophils. Under the quasi steady state conditions of this study the kinetics of granulocytes in the present CLL patients appeared to be normal, despite a marked lymphocytic infiltration of the bone marrow. The apparent discrepancy between these findings and the data obtained with autotransfusion of DFP-labeled granulocytes is discussed.

Aged↗
PubMed1990

Differential mechanisms in the stimulus-secretion coupling in human basophils: evidence for a protein-kinase-C-dependent and a protein-kinase-C-independent route.

Upon activation, basophilic granulocytes release inflammatory mediators, such as histamine. We studied histamine release (HR) of purified (64 +/- 10%) human basophils after cross-linking of membrane-bound IgE via anti-IgE or after binding of the chemoattractant formyl-methionyl-leucyl-phenylalanine (FMLP). A variability in the extent of histamine release upon stimulation by either anti-IgE or FMLP was found between donors. Non-responders for FMLP showed high histamine release for anti-IgE, and vice versa. Inhibition of protein kinase C (PKC) by staurosporine (STSP) resulted in partial inhibition of the anti-IgE-induced HR, whereas inhibition of a PKC-independent pathway by wortmannin (WTM) totally blocked the anti-IgE induced histamine release. The HR induced by FMLP was not affected by either of these inhibitors. We conclude that major differences exist in the signal-response coupling between the anti-IgE and FMLP-induced HR in human basophils. The so-called releasability of human basophils may be due to the availability of different cell activation pathways.

Alkaloids↗
PubMed1985

Activation of human basophils by Staphylococcus aureus Cowan I. II. Alternative F(ab')-mediated mechanism.

We investigated the capacity of Staphylococcus aureus Cowan I (Cowan Staph A+) and Staphylococcus aureus Wood 46 (Wood Staph A-) to induce histamine release from human basophils in vitro. Cowan Staph A+ (3 X 10(6) to 3 X 10(8)/ml), which synthesizes protein A (Staph A), stimulated the release of histamine from basophils, whereas Wood Staph A- (3 X 10(6) to 3 X 10(9)/ml), which does not synthesize Staph A, did not induce histamine secretion. Soluble Staph A (10(-3) to 10 micrograms/ml) also induced histamine secretion from human basophils, Hyperiodination of Staph A, which destroys over 90% of the original Fc reactivity without altering the Fab binding site, did not alter this protein's ability to induce histamine release. The stimulating effect of Staph A was suppressed by preincubation with human polyclonal IgG and a human monoclonal IgM, which have F(ab')-Staph A reactivity. In contrast, rabbit IgG and a human monoclonal IgM possessing only Fc-Staph A reactivity did not inhibit Staph A activity. Preincubation with Staph A or Cowan Staph A+ resulted in complete cross-desensitization to a subsequent challenge with homologous and heterologous stimuli. These results indicate that Staph A and Cowan Staph A+ activate human basophils by interacting with the F(ab')2 region of IgE and/or IgG present on the cell surface.

Basophils↗
PubMed1986

Passive in vitro sensitization of human basophils with Dermatophagoides farinae specific IgE.

Basophils from allergic or non-atopic donors were depleted for their native membrane IgE by acid treatment and then passively sensitized by Dermatophagoides farinae specific IgE containing sera. Histamine release experiments were performed with a highly purified allergen (Df 11) on native cells, acid treated cells and passively sensitized cells. In the sensitization procedure, the quantity of the basophil-bound serum IgE is dependent on the concentration of the sensitizing serum IgE and the histamine release capacity is specifically acquired. It is shown that after passive sensitization basophil membrane IgE density as well as basophil sensitivity to Df 11 in histamine release experiments depend on the ratio [Df 11 specific IgE/total IgE] in the sensitizing serum.

Allergens↗
PubMed1987

Basophil sensitivity and reactivity to monoclonal anti-human IgE after in vitro sensitization with human myeloma IgE.

Leucocytes from human peripheral blood were acid eluted and sensitized in vitro with increasing concentrations of radiolabelled myeloma IgE. This sensitization step was performed with or without 30% IgE depleted serum. After the IgE binding, cells were washed and submitted to a challenge with monoclonal anti-IgE for the determination of the cellular sensitivity and reactivity in a histamine release assay. A sample of each of the sensitized cells was analyzed for its radioactivity and the number of basophils quantified, thus allowing the determination of the mean number of IgE molecules per basophil. Raising the IgE concentrations in the sensitization procedure led to an increase of the IgE on the basophil membrane, and to a concomitant elevation of the cell sensitivity. The presence of serum during the binding of IgE onto the cells lowers slightly the binding of IgE to the basophils but decreases strongly the cellular reactivity.

Antibodies, Anti-Idiotypic↗
PubMed2002

Analyzing the roles of mast cells and basophils in host defense and other biological responses.

The sudden and systemic activation of mediator release from mast cells and basophils that can occur when some sensitized subjects are challenged by minute amounts of specific antigen (eg, from an insect sting or peanuts) can result in fatal anaphylaxis, a reaction that arguably represents the most grotesque imbalance between the cost and benefit of an immune response. Why then do mast cells and basophils continue to exist and, in the case of mast cells, populate almost all vascularized tissues? This review will consider the roles of mast cells and basophils in health and disease, emphasizing particularly their proven or potential functions in host defense. We will also describe briefly some approaches to investigate mast cell and basophil functions in vivo, including the use of mast cells generated directly from embryonic stem cells in vitro.

Animals↗
PubMed2004

The effect of nicotine on basophil histamine release.

BACKGROUND: Changes in the immune and inflammatory response are induced by smoking tobacco but underlying mechanisms remain to be elucidated. OBJECTIVE: This study investigated the effect of nicotine agonists on histamine release from human basophils. METHODS: Peripheral blood basophils were obtained from healthy volunteers. The effect of the nicotine agonists [-]-1-methyl-2-[3-pyridyl]pyrrolidine and (+)-nicotine di-p-toluoyltartrate salt on cell viability and anti-IgE induced histamine release was investigated. RESULTS: Cell viability was not altered by preincubation with the agents for 15 min. Anti-IgE induced histamine release was significantly inhibited by preincubation (15 min, 37 degrees C) with [-]-1-methyl-2-[3-pyridyl]pyrrolidine at the highest concentration tested 10(-)3 M (p<0.01). Preincubation (15 min, 37 degrees C) with (+)-nicotine di-p-toluoyltartrate salt significantly inhibited anti-IgE induced histamine release at 10(-3)M and 10(-5) M (p<0.05). CONCLUSIONS: This study has demonstrated that nicotine agonists inhibit histamine release from human basophils. Further studies examining the effect of smoking on basophil activation are required.

Adult↗
PubMed1998

The effect of tyrosine kinase inhibitors on IgE-mediated histamine release from human lung mast cells and basophils.

OBJECTIVE AND DESIGN: To investigate the role of tyrosine kinases (TK) in IgE-mediated signal transduction in human lung mast cells (HLMC) and basophils. MATERIALS: Peripheral blood basophils (n > or = 4) and human lung mast cells (n > or = 6). TREATMENT: Cells were preincubated with TK inhibitor for 15 min at 37 degrees C, before the addition of anti-IgE. METHODS: Histamine release (HR) was assayed using a fluorimetric technique. Results were compared using nonparametric statistics. RESULTS: Piceatannol and ST638 significantly (p < or = 0.05) inhibited anti-IgE induced HR from HLMCs and basophils whilst lavendustin C had no effect in either cell type. Herbimycin A also significantly (p < or = 0.05) inhibited anti-IgE induced HR from both cell types, an effect which was dose dependent but did require a 16 h preincubation with drug. CONCLUSIONS: In summary, HLMCs and basophils exhibit distinct inhibitory profiles in the presence of various inhibitors of TK.

Basophils↗
PubMed2000

Effects of protein kinase C and phospholipase C inhibitors on IgE-dependent and IgE-independent basophil histamine release.

OBJECTIVE AND DESIGN: This study was aimed to evaluate the effects of two protein kinase C (PKC) inhibitors (staurosporine and chelerythrine) and one phospholipase C (PLC) inhibitor (U73122) on basophil histamine release induced by anti-IgE, N-formyl-methionyl-leucyl-phenylalanine (FMLP), IL-3 and GM-CSF. METHODS: Leukocytes were suspended in solutions containing physiological or low Na+ concentrations, since IL-3 and GM-CSF were shown to induce histamine release only when the inhibitory effect of extracellular Na+ has been removed. After incubation with PKC and PLC inhibitors, the stimuli were added and histamine release was measured by an automated fluorometric method. RESULTS: Staurosporine and chelerythrine exerted a significant inhibitory effect on histamine release induced by anti-IgE, IL-3 and GM-CSF at concentrations much higher than those required to inhibit PKC. FMLP-induced histamine release in a physiological Na+-containing medium was not significantly modified by staurosporine, although it was reduced by high concentrations of chelerythrine. A slight inhibition by high concentrations of staurosporine was found when basophils were suspended in a low Na+ medium. U73122 exerted a significant and dose-dependent inhibitory effect on basophil histamine release induced by anti-IgE, FMLP, IL-3 and GM-CSF. CONCLUSION: These results suggest that a prodegranulatory role of PKC in basophil histamine release induced by anti-IgE, FMLP, IL-3 and GM-CSF is unlikely; conversely, it is conceivable that PLC has a role in signal transduction and histamine release induced by the above stimuli.

Alkaloids↗
PubMed1992

12-Lipoxygenase from rat basophilic leukemia cells, an oxygenase with leukotriene A4-synthase activity.

Rat basophilic leukemia cells exhibit 12-lipoxygenase activity only upon cell disruption. 12-Lipoxygenase may also possess 15-lipoxygenase activity, as is indicated by the formation of low amounts of 15(S)-HETE, in addition to the predominant product 12(S)-HETE, upon incubation of partially purified 12-lipoxygenase with arachidonic acid. With 5(S)-HPETE as substrate not only 5(S), 12(S)-diHETE and 5(S), 15(S)-diHETE are formed, but also LTA4, as was indicated by the presence of LTA4-derived LTB4-isomers. 12-Lipoxygenase from rat basophilic leukemia cells has many features in common with 12-lipoxygenase from bovine leukocytes. As was suggested for the latter enzyme, 12-lipoxygenase from rat basophilic leukemia cells may represent the remaining LTA4-synthase activity of 5-lipoxygenase, of which the 5-dioxygenase activity has disappeared upon cell disruption. Such a possible shift from 5-lipoxygenase activity to 12-lipoxygenase activity could not simply be induced by interaction of cytosolic 5-lipoxygenase with a membrane fraction after cell disruption, but may involve release of membrane-associated 5-lipoxygenase upon disruption of activated rat basophilic leukemia cells.

Animals↗
PubMed1987

Experiments on the mode of action of piriprost (U-60,257), an inhibitor of leukotriene formation in cloned mouse mast cells and in rat basophil leukemia cells.

We studied the effect of piriprost, an inhibitor of sulfidopeptide leukotriene (LT) formation, on the generation of the known products of the 5-lipoxygenase pathway of arachidonate metabolism in calcium ionophore A23187-challenged rat basophil leukemia cells and cloned, growth factor-dependent, mouse mast cells. Piriprost inhibited the formation of 5-hydroxyeicosatetraenoic acid (5-HETE), and LTB4, and the sulfidopeptide leukotrienes (LTC4 in the mouse mast cells and both LTC4 and a mixture of LTD4 and LTE4 in the rat basophil leukemia cells) in parallel (IC50 values ranged between 9 and 14 microM for the mouse mast cells and between 15 and 50 microM for the basophil leukemia cells). Our previous observation that piriprost is only a very weak inhibitor of the solubilized LTC synthase of rat basophil leukemia cells was extended to similar enzyme preparations derived from the mouse mast cells (IC50 1.5 mM). The results are consistent with the conclusion that piriprost acts as an inhibitor of the 5-lipoxygenase reaction and that its activity in intact cells is not likely to involve the inhibition of the LTC synthase.

Animals↗
PubMed1989

Inhibition by adenosine of histamine and leukotriene release from human basophils.

Adenosine inhibited the release of histamine and leukotriene C4 (LTC4) from immunologically-activated basophils in a dose-dependent manner. Structural congeners of adenosine also attenuated the elaboration of these two mediators from stimulated basophils and a rank order of potency for the inhibition was observed following the sequence 2-chloroadenosine greater than or equal to N-ethylcarboxamidoadenosine (NECA) greater than adenosine greater than or equal to R-phenylisopropyladenosine (R-PIA) greater than or equal to S-PIA. These same nucleosides modulated the generation of LTC4 more potently than the release of histamine. A number of methylxanthines, which are antagonists of cell surface adenosine receptors, reversed the inhibition by adenosine and its congeners of the release of both histamine and LTC4 to varying extents. Dipyridamole and nitrobenzylthioinosine (NBTI), agents that block the intracellular uptake of adenosine, antagonized the inhibition of histamine release by adenosine (and 2-chloroadenosine) but failed to reverse the attenuation of LTC4 generation by the nucleoside. These same uptake blockers were unable to antagonize the inhibitory effects of NECA on either histamine or LTC4 release. In purified basophils, NECA and R-PIA, and in that order of decreasing reactivity, increased total cell cyclic adenosine monophosphate (cAMP) levels and inhibited the stimulated release of mediators. In total, these results suggest that the basophil possesses a cell surface adenosine receptor which, on the basis of both pharmacological and biochemical criteria, most closely conforms to an A2/Ra-like receptor. However, in addition to an interaction at the cell surface, studies with agents that block the intracellular uptake of adenosine suggest that the nucleoside may also exert intracellular effects when countering the release of histamine (but not LTC4).

2-Chloroadenosine↗
PubMed1990

Basophils in skin reactions of mast cell-deficient mice infested with Dermacentor variabilis.

Acquired resistance to ticks in guinea pigs has been found to be associated with basophil-rich skin reactions. Mice, which are generally believed to possess few, if any basophils, also acquire resistance following repeated tick infestations and this has been found to be associated with increased numbers of dermal mast cells. Mast cell-deficient W/Wv mice have, however, also been shown capable of acquiring resistance after two infestations with Dermacentor variabilis larvae. In the studies described here, we have examined, with the electron microscope, skin reactions in W/Wv and +/+ mice undergoing their third infestation with Dermacentor variabilis. Basophils, along with neutrophils and eosinophils, were identified using established criteria. The possibility that basophils contribute to various pathogenetic mechanisms in these and other strains of mice is discussed.

Animals↗
PubMed1984

Isolation of guinea pig basophils using anti-leukocyte antibody and density gradient centrifugation on Percoll.

Peripheral blood basophils were isolated from guinea pigs using a 2-step procedure. Initial enrichment of basophils was achieved by treating leukocyte preparations obtained from whole blood with antibody to contaminating granulocytes and mononuclear cells. Basophil populations of 82% purity (mean; range 65-99%) were obtained by subsequent application of the antibody treated preparation to discontinuous Percoll gradients. The isolated basophils were viable and shown to be functional by histamine release upon stimulation with various secretogogues.

Animals↗
PubMed1986

A flow cytometric procedure for the isolation of antigenically responsive human basophils.

A flow cytometric procedure is described for the isolation of human basophils. The basophils are isolated by cell sorting after passive sensitization with mouse FITC-IgE anti-DNP, and the isolated basophils exhibit characteristic histamine release in response to incubation with DNP21-human serum albumin conjugates. Using this method, 1-4 X 10(5) basophils can be isolated at greater than or equal to 98% purity from approximately 30 ml whole blood in a 2 h sorting procedure.

Basophils↗
PubMed1987

A rapid Percoll technique for the purification of human basophils.

We have refined a rapid single-step Percoll technique to obtain a basophil-enriched mononuclear cell fraction suitable for further purification. Greater than 75% of the total blood basophils were recovered from a blood-Percoll interface at a purity of between 5 and 23%. The contaminating cells were principally lymphocytes with a smaller (20-25%) percentage of monocytes. Further purification using the penicillin affinity column led to the recovery of between 28 and 64% of the total blood basophils at purities ranging from 52 to 92%, a substantial improvement over our earlier protocol. There was also a marked increase in the recovery of basophils from the affinity column over our previous technique, which lead to a moderate (5-10%) increase in overall recovery.

Basophils↗