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At least 1,675 records · Page 93Linked to original sources
PubMed1991

Tyrosine phosphorylation is an early signaling event common to Fc receptor crosslinking in human neutrophils and rat basophilic leukemia cells (RBL-2H3).

Phosphotyrosine-containing proteins were detected by western blotting of whole cell lysates of purified human neutrophils or rat basophilic leukemia cells (RBL-2H3) using a polyclonal anti-phosphotyrosine antibody. When either cell type was stimulated with the appropriate Fc crosslinking agent, heat-aggregated IgG for the neutrophil or DNP-HSA for the IgE-sensitized RBL-2H3, a rapid increase in the phosphotyrosine content of several proteins was observed. The kinetics and specificity of both responses suggest that Fc receptor crosslinking activates a receptor-associated tyrosine kinase, probably a member of the src family of tyrosine protein kinases. The subsequent tyrosine phosphorylation events are likely to be important in Fc receptor-mediated stimulus-response coupling in inflammatory cells.

Animals↗
PubMed1982

Nonpolar lipid methylation-identification of nonpolar methylated products synthesized by rat basophilic leukemia cells, retina and parotid.

Incorporation of radioactivity from [3H- or 14C-methyl] methionine into nonpolar lipids had been investigated in rat basophilic leukemia (RBL) cells, retina, and rat parotid gland. These nonpolar methylated lipids were extracted into heptane and characterized by thin-layer chromatography, high performance liquid chromatography, gas chromatography, and mass spectrometry. The major methylated nonpolar lipid product in the RBL cells themselves was ubiquinone-9, which accounted for about 90% of the nonpolar lipid and 20-30% of the total radioactive lipid formed. There was a modest increase in the methylation of nonpolar lipids upon stimulation of the RBL cells with IgE and anti-IgE, but the significance of this change is uncertain. In contrast to whole cells, RBL membrane fractions (incubated with [3H-methyl]-S-adenosylmethionine) incorporated radioactivity primarily into fatty acid methyl esters and not ubiquinone. A third product, 2-(methylthio)-benzothiazole, was formed by RBL cells, retina and minced parotid upon incubation in enriched media. This product was formed enzymatically, apparently by the known enzyme S-thiolmethyltransferase, using the thiol substrate which contaminates these media. Evidence suggest that the enzyme may reside, at least in part, on the surface of the cells.

Animals↗
PubMed1983

The relationship between cyclic AMP changes and histamine release from basophil-rich human leucocytes.

Histamine release and changes in cyclic AMP levels induced by a variety of stimuli have been measured in isolated human leucocytes from a patient with 40-70% basophilia. Adenosine and sodium fluoride induced early monophasic rises in cyclic AMP which peaked at 1 min, but they did not release histamine. 2',5'-Dideoxyadenosine (DDA) caused a transient fall in cyclic AMP levels. Anti-IgE, polylysine and calcium ionophore A23187 induced a slow release of histamine commencing 2-5 min after addition of secretagogue. With polylysine and A23187, release was still proceeding 45 min after challenge. In contrast, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (f-met-leu-phe) induced a rapid secretion of histamine which was complete within 2 min. Anti-IgE induced a rapid monophasic rise in cyclic AMP which reached a maximum at 45 sec and was inhibited by pretreatment with DDA. Cyclic AMP rises induced by polylysine and f-met-leu-phe were kinetically similar but smaller in magnitude. A23187 caused a later rise in cyclic AMP which peaked 3 min after challenge. A high concentration (50 microM) of compound 48/80 induced a slow cytotoxic release of histamine which was not accompanied by changes in cyclic AMP levels. The inconsistent quantitative and kinetic relationships of histamine release and cyclic AMP production suggest that changes in cyclic AMP levels may not play a key role in the biochemical events leading to mediator secretion from human basophil leucocytes.

Adenosine↗
PubMed1983

Inhibition of the A-23187-stimulated leukotriene and prostaglandin biosynthesis of rat basophil leukemia (RBL-1) cells by nonsteroidal anti-inflammatory drugs, antioxidants, and calcium channel blockers.

Rat basophil leukemia cells (RBL-1), when grown in monolayer, synthesize from endogenous substrates the prostaglandins (PG) E2, F2 alpha, and I2 (measured as 6-keto-PGF1 alpha) and 6-sulfidopeptide-containing leukotrienes (SRS), as well as materials that react serologically with anti-12-hydroxyeicosatetraenoic acid (HETE). The non-steroidal anti-inflammatory drugs indomethacin and aspirin inhibited PGE2 synthesis by RBL-1 cells, which had been stimulated with the calcium ionophore A-23187, in a dose-dependent manner with an IC50 of 0.7 and 7.8 microM respectively. Indomethacin, when used at higher concentrations, also inhibited iSRS synthesis with an IC50 of 230 microM. Benoxaprofen, also a non-steroidal anti-inflammatory drug, inhibited both PGE2 and iSRS production in a dose-dependent manner, but inhibition of the iSRS biosynthesis was three times more effective than inhibition of PGE2 production. The anti-oxidants gossypol, butylated hydroxyanisole (BHA), nordihydroguariatic acid (NDGA), and 3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline (BW755c) also inhibited iSRS synthesis more effectively than PGE2 biosynthesis. The IC50 values for inhibition of iSRS production were 0.2 microM (gossypol), 0.5 microM (BW755c), 0.6 microM (BHA), and 0.6 microM (NDGA) compared to 2.8 microM (gossypol), 2.0 microM (BW755c), 4.8 microM (BHA) and 2.6 microM (NDGA) for inhibition of PGE2 synthesis. Gossypol, BW755C, BHA, and NDGA, as well as benoxaprofen, inhibited i12-HETE-biosynthesis (IC50 for gossypol, 0.32 microM; and for benoxaprofen, 0.5 microM). Two calcium channel blockers, verapamil and nifedipine, inhibited PGE2, iSRS and i12-HETE synthesis in a dose-dependent manner. The calcium channel blockers inhibited iSRS synthesis ten times more effectively than PGE2 production.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Flavonoid inhibition of human basophil histamine release stimulated by various agents.

Eleven naturally occurring flavonoids representing five different chemical classes were studied for their effects on human basophil histamine release triggered by six different stimuli. The flavonoids included flavone, quercetin, taxifolin, chalcone, apigenin, fisetin, rutin, phloretin, tangeretin, hesperetin, and naringin. The stimuli were antigen, anti-IgE, concanavalin A, ionophore A23187, formylmethionylleucylphenylalanine, and tetradecanoyl phorbol acetate. Concentration-effect relationships were established for each flavonoid (5-50 microM) at concentrations of stimuli which produced near optimal histamine release. Variable degrees of inhibition were noted depending on the nature of the stimulus and flavonoid structure. The flavonols, quercetin and fisetin, and the flavone, apigenin, exhibited a predilection to inhibit histamine release stimulated by IgE-dependent ligands (antigen, anti-IgE, and con A). The flavanone derivatives, taxifolin and hesperetin, were inactive, as were the glycosides, rutin and naringin. The open chain congeners, chalcone and phloretin, also possessed inhibitory activity. Thus, the flavonoids may be useful probes in comparative analysis of secretory phenomena. The findings suggest that the biochemical pathways leading to secretion differ subtly from one stimulus to another. The differences are detectable with flavonoids of different structures and possibly reflect distinct pathways of Ca2+ mobilization or other unique mechanisms of action.

Arachidonic Acid↗
PubMed1986

Inhibition of the leukotriene synthetase of rat basophil leukemia cells by diethylcarbamazine, and synergism between diethylcarbamazine and piriprost, a 5-lipoxygenase inhibitor.

Diethylcarbamazine inhibited the formation of sulfidopeptide leukotrienes in rat basophil leukemia (RBL) cells (50% inhibitory concentration, EC50, 3 mM). Similar concentrations also inhibited the formation of leukotriene C4 (LTC4) by LTC synthetase, a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling LTA4 to glutathione. By contrast, the conversion of LTA4 to LTC4 using enzymes from rat liver was at least ten times less sensitive to this inhibitor. The EC50 for inhibition of the leukotriene C synthetase of RBL cells was directly proportional to the LTA4 concentration in the incubations, ranging from 1.5 mM at 10 microM LTA4 to over 40 mM at 500 microM LTA4. Kinetic analysis revealed that the inhibition of the leukotriene C synthetase reaction by diethylcarbamazine was competitive with respect to LTA4. In contrast to diethylcarbamazine, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the 5-lipoxygenase step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells. On the other hand, low concentrations of piriprost, which had no demonstrable inhibitory activity on leukotriene formation by themselves, markedly synergized the inhibitory activity of diethylcarbamazine. These results are consistent with the interpretation that both piriprost and diethylcarbamazine inhibit leukotriene formation but that they act on sequential steps in the biosynthetic pathway in such a manner as to synergistically interfere with the availability or utilization of LTA4 in the leukotriene C synthetase reaction.

Animals↗
PubMed1993

Effect of okadaic acid on human basophil secretion.

We examined the effects of a phosphatase inhibitor, okadaic acid, on mediator secretion from human basophils. These cells are known to respond to a number of stimuli that appear to utilize distinct biochemical pathways converging on mediator release. Okadaic acid was found to inhibit IgE-mediated release (histamine release inhibited 80 +/- 12% and leukotriene release inhibited 100% following a 10-min preincubation with okadaic acid and stimulation with an optimal concentration of anti-IgE antibody) at a concentration of 1 microM. The concentration-response curve to okadaic acid was steep, with 0.1 microM yielding only 20 +/- 10% inhibition of either mediator. Secretion following stimulation with the univalent stimulus, fMet-Leu-Phe peptide, was not inhibited by okadaic acid. Unlike cAMP-active agents that inhibit cytosolic Ca2+ elevations following IgE-mediated stimulation, the increased state of cellular protein phosphorylation, which presumably results from treatment with 1 microM okadaic acid, had no effect on the elevations in free cytosolic Ca2+ that follow stimulation with anti-IgE antibody of fMet peptide.

Basophils↗
PubMed1986

Antibody enhances lymphocyte proliferation in guinea pigs immunized to express cutaneous basophil hypersensitivity.

Lymphocytes from HSA-sensitized guinea pigs expressing cutaneous basophil hypersensitivity (CBH) proliferate in the presence of specific antigen. We report that this proliferative response is enhanced by the addition of anti-HSA antibody, either in the form of whole immune serum or as purified antibody. The enhancement was characterized as a marked shift of the antigen dose-response curve such that significant [3H]thymidine incorporation was observed at antigen concentrations much lower than those eliciting a comparable response in the absence of immune serum. Enhancement was antigen specific and required an intact immunoglobulin molecule. Antibodies capable of enhancing antigen-specific lymphocyte proliferation could be isolated from serum by affinity chromatography as early as 7 days after sensitization and were also evident in sera obtained at later intervals. It is unlikely that such antibodies account for the progressive decline of CBH reactivity and they may actually influence its initial expression.

Animals↗
PubMed1985

A mathematical model to quantitate histamine release from basophils challenged in vitro with insect venom.

Using a two parameter mathematical model, it was possible to describe clinically obtained data from histamine release (HR) in vitro as a response to basophils challenged by insect venom. The Gompertz function used in this model not only reflects the observed HR data but can be used to predict maximal HR values from initial lower antigen concentrations HR determinations. The model was used to calculate the concentration of venom antigens releasing 25% of total intracellular histamine (HR25). This is clinically significant in that while knowledge of the HR25, or any other reference fraction, facilitates comparisons between allergic patients, it is impossible to empirically administer venom antigen concentrations that will produce exactly HR25 in a given clinical setting.

Adult↗
PubMed1980

Modulation of the rate of histamine release from basophils by cyclic AMP.

Rates of histamine release from human basophil leukocytes have been studied in response to three different stimuli: antigen, ionophore A23187 and strontium ions. Dibutyryl cycle AMP and other agents which are assumed to cause a rise in intracellular levels of cyclic AMP accelerate the release of histamine induced by all of the stimuli. In addition, dibutyryl cyclic AMP caused an inhibition of the maximum release obtainable with antigen stimulation but no inhibition of the maximum release obtainable with ionophore A 23187 or with strontium ions alone.

Basophils↗
PubMed1988

Leukotriene D4-induced activation of protein kinase C in rat basophilic leukemia cells.

We studied the subcellular distribution of protein kinase C (PKC) in the particulate and cytosolic fractions of rat basophilic leukemia (RBL-1) cells treated with leukotriene D4 (LTD4) and compared these results with those of phorbol myristate acetate (PMA). Consistent with the earlier reports, treatment of RBL-1 cells with PMA resulted in a time- and dose-dependent translocation of PKC from cytosolic to the particulate fractions, sustained for at least 10 min. When RBL-1 cells were treated with LTD4, a small, transient decrease in PKC activity in cytosolic fraction was observed within 7.5 s after LTD4 treatment. This was accompanied by a significant increase of PKC in the particulate fraction. However, at 15 and 30 s, both particulate and cytosolic PKC activities were increased with LTD4 treatment. The activation induced by LTD4 was dose- and time-dependent with maximal effects occurring within 30 s, declining at the later time points. Pretreatment of the cells with 2(R)-hydroxy-3(S)-carboxyethylthio-3-[2-(8-phenyloctyl,pheny l]propanoic acid (SK&F 104353), a high affinity specific LTD4 receptor antagonist, and also with staurosporine, a potent inhibitor of PKC, completely inhibited the LTD4-induced activation of PKC both in the particulate and cytosolic fractions. These results suggest that activation of PKC by LTD4 is different from that elicited by PMA. The ability of SK&F 104353 to block LTD4-induced activation of PKC further suggests that stimulation of PKC might be an important intermediate step in the signal transduction mechanism of the LTD4 receptor in RBL-1 cells.

Animals↗
PubMed1991

Expression of an inwardly rectifying K+ channel from rat basophilic leukemia cell mRNA in Xenopus oocytes.

Rat basophilic leukemia cells (RBL-2H3) have previously been shown to contain a single type of voltage-activated channel, namely an inwardly rectifying K+ channel, under normal recording conditions. Thus, RBL-2H3 cells seemed like a logical source of mRNA for the expression cloning of inwardly rectifying K+ channels. Injection of mRNA isolated from RBL-2H3 cells into Xenopus oocytes resulted in the expression of an inward current which (1) activated at potentials negative to the K+ equilibrium potential (Ek), (2) decreased in slope conductance near Ek, (3) was dependent on [K+]o and (4) was blocked by external Ba2+ and Cs+. These properties were similar to those of the inwardly rectifying K+ current recorded from RBL-2H3 cells using whole-cell voltage clamp. Injection of size-fractionated mRNA into Xenopus oocytes revealed that the current was most strongly expressed from the fraction containing mRNA of approximately 4-5 kb. Expression of this channel represents a starting point for the expression cloning of a novel class of K+ channels.

Animals↗
PubMed1988

Basophilic leukemia and the hypersecretion of gastric acid and pepsin.

A 48-yr-old man with chronic myelogenous leukemia and basophilia developed a duodenal ulcer and hemorrhage. Gastric analysis revealed basal hyper-secretion of acid (33.1 mEq/h) and pepsin (44.5 x 10(-4) peptic units/h). Blood, serum, and urine histamine was elevated and serum gastrin was normal. Although acid output was markedly suppressed with ranitidine (50 mg i.v.), pepsin secretion was only inhibited 63% and had returned to basal levels by the sixth hour. Maximal acid output does not suggest a trophic effect of histamine in this patient. The previously reported cases of basophilic leukemia and gastric hypersecretion or duodenal ulcer disease are reviewed.

Basophils↗
PubMed1992

Basophil degranulation control.

We first present a global simulation model describing inhibition of human basophil degranulation by means of high dilutions. Then we study an optimal control problem associated to a non-linear compartmental model. This control is associated to an antigen concentration. For solving this control problem we used a dynamic programming method.

Basophil Degranulation Test↗
PubMed1984

Effect of cholera enterotoxin on calcium uptake and cyclic AMP accumulation in rat basophilic leukemia cells.

Cholera enterotoxin (CT), at an optimal concentration of 2.38 X 10(-10) M, stimulated calcium uptake (P less than 0.01) and cyclic AMP accumulation (P less than 0.02) in cultured rat basophilic leukemia cells. No significant effect of CT on calcium release or cyclic GMP accumulation was detected. Pharmacologic and chemical agents which block calcium uptake or prostaglandin synthesis antagonized the effect of CT.

Animals↗
PubMed1987

Basophilic leukaemia in a dog.

Leukaemia in an 11-year-old bitch was characterized by the presence in the peripheral blood and bone marrow of cells with lobulated nuclei and numerous metachromatic cytoplasmic granules. The results of cytochemical stains for peroxidase and naphthol AS-D chloracetate esterase activity were negative. Ultrastructurally, the cytoplasmic granules were finely granular with no membranous coils or crystalline lattice structures. Based on these findings, the neoplastic cells were classified as basophils.

Animals↗
PubMed1976

Identification of basophilic granulocytes in human leukocyte suspensions subjected to immunofluorescence procedures with anti-IgE.

A method is described by which human leukocyte preparations obtained by Ficoll-Isopaque centrifugation are stained and fixed in such a way that the basophilic granulocytes in these preparations can be identified when the latter are subjected to immunofluorescence procedures with anti-IgE. Capping, blocking and absorption experiments confirmed the specificity of the test.

Antibodies, Anti-Idiotypic↗