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At least 955 records · Page 53Linked to original sources
PubMed1996

Quantitation of 1-stearoyl-2-arachidonoyl-sn-3-glycerol in human basophils via gas chromatography-negative ion chemical ionization mass spectrometry.

Investigation of the role of diacylglycerol molecular species in signal transduction in human basophils has been impeded by the lack of an assay method with adequate sensitivity and selectivity. Conversion of 1-stearoyl-2-arachidonoyl-sn-3-glycerol to the pentafluorobenzoyl ester conveys electron-capture properties to the diacylglycerol. The electron-capture derivative of the diacylglycerol is amenable to gas chromatographic analysis and undergoes limited fragmentation under negative ion mass spectrometric conditions with generation of an intense molecular anion at m/z 838. Monitoring m/z 838 for detection of 1-stearoyl-2-arachidonoyl-sn-3-glycerol and m/z 841 for detection of 1-trideuterostearoyl-3-arachidonoyl-sn-2-glycerol employed as the internal standard provides the analytical basis for GC-MS quantitation of the endogenous diacylglycerol in human basophils. The assay displays excellent reproducibility over a wide range of concentrations with variations < or = 10%. The GC-MS assay is highly selective and exquisitely sensitive with a detection limit of < or = 0.20 pg (approximately 30 fmol) for endogenous 1-stearoyl-2-arachidonoyl-sn-3-glycerol per injection. Approximately 400 fmol of the diacylglycerol were extracted from 10(5) stimulated human basophils.

Basophils↗
PubMed1994

Lipopolysaccharide primes human basophils for enhanced mediator release: requirement for plasma co-factor and CD14.

Lipopolysaccharide (LPS) is known to enhance IgE-mediated basophil degranulation. Recently, the complex of LPS and plasma LPS-binding protein(LBP) has been shown to induce secretory response via CD14 in monocytes and neutrophils. In the current study, we observed that the sensitivity to LPS of basophils was increased to 100-fold by co-incubation with plasma. LPS promptly completed its effect and amplified degranulation by stimuli bypassing IgE-receptors. Treatment with anti-CD14 completely abolished the priming effect of LPS. These results indicate that the priming effect of LPS on basophil mediator release is mediated via CD14, and that plasma co-factor, possibly identical to LBP, potentiates this reaction.

Acute-Phase Proteins↗
PubMed1996

Inhibition of basophil histamine release by a haptenic peptide mixture prepared by chymotryptic hydrolysis of wheat flour.

For application to the treatment of wheat-sensitive allergy, we developed a practical method for producing a haptenic peptide mixture, and evaluated its haptenic properties. Wheat flour was hydrolyzed with chymotrypsin to obtain a hydrolysate, and the diffusible fraction from the hydrolysate was subjected to gel-filtration. The resulting oligopeptide fraction could bind to wheat-specific IgE antibodies in the serum of patients allergic to wheat. Since this peptide mixture did not induce histamine release from basophils in these patients, it was concluded that the peptide mixture was composed of monovalent haptens. Histamine release from antigenstimulated basophils was almost completely inhibited when the basophils were preincubated with the haptenic peptide mixture. These results suggest that this haptenic peptide mixture can regulate the allergenic reaction in an epitope-specific manner.

Basophils↗
PubMed1977

Basophilic cells in allergic nasal secretions.

Evidences on the important role of tissue mast cells in inducing allergy have accumulated. There cells are known to be present in nasal secretion but have not been well studied. In the present study basophilic cells containing granules which stained metachromatically appeared in the nasal secretion in various kinds of inhalant allergy. An increase in their number was observed after nasal provocation and during the pollinosis season and showed a decrease after a course of immunotherapy or during the off-season of pollinosis. They were well correlated in degree with nasal symptoms, nasal eosinophilia, and nasal provocative reactions. These results suggest that the appearance of the basophilic cell in nasal secretion is related to their specifity in nasal allergy. The possibility of onset of nasal allergy due to the release of chemical mediators from basophilic cells in nasal secretion was discussed.

Adolescent↗
PubMed1975

An autoradiographic study of human blood basophils.

The aim of this paper is the selective visualization of human blood basophils in autoradiographs. [(3)H]Thymidine-labelled basophils in buffy coat smears were fixed in methanol-formaldehyde follwed by 5-aminoacridine hydrochloride and stained with basic Aldehyde Fuchsin prior to autoradiographic processing. The technique described represents a simple method for quantitative autoradiographic studies on basophil kinetics and the interaction of these cells with IgE-mediated atopias.

Acridines↗
PubMed1995

Ultrastructure of proteoglycans in the specific granules of guinea-pig basophilic leukocytes as demonstrated by cuprolinic blue staining.

The ultrastructure of sulphate proteoglycans in basophil granules was examined using cytochemical procedures designed to stabilize and visualize these highly anionic macromolecules in situ. Unfixed or glutaraldehyde-prefixed guinea-pig spleen cells were submitted to fixation/staining in 2.5% glutaraldehyde, 0.2% cuprolinic blue (CB; a cationic phthalocyanin dye) and 0.2 or 0.3 M MgCl2 with or without glycosidase treatments. Abundant electron-dense precipitates were present throughout the granule matrix. The stained structures were often arranged in a quasi-crystalline typical banded pattern. Negative control basophils had no electrondense precipitates. Digestion with chondroitinase ABC destroyed the CB-positive electron-dense banded or filamentous patterns while sialidase treatment did not, but led to larger CB-positive filaments in the cytoplasm near the granules. Taking into account their high anionicity, as shown by the stability of dye binding in the presence of 0.3 M MgCl2, and their susceptibility to chondroitinase ABC, the CB-precipitates are assumed to be related to the sulphated proteoglycans previously characterized in basophil granules. The CB-positive crystalline or filamentous network of the granule matrix is also assumed to reflect the in situ location and organization of these intracellular proteoglycans and may be involved in maintaining the shape of the granule.

Animals↗
PubMed1975

[5-Aminoacridine hydrochloride for fixation of human blood basophils (author's transl)].

5-aminoacridine hydrochloride (0.4 percent in 50 percent aqueous ethanol) proved to be a useful fixative for the preservation of human blood basophils pretreated with methanol-formaldehyde (9:1 V/V). Leaching of the water-soluble basophil granules or other artificial cell alterations common to fixatives in current use were not observed. The organic compound used did not induce any chemographic artifacts in nuclear tracers, in contrast to most of the other fixatives hitherto applied. 5-aminoacridine hydrochloride is therefore particularly suitable for autoradiography of the human blood basophils.

Acridines↗
PubMed1975

[Autoradiographic demonstration of human basophils].

A new technique is described which enables a selective tinctorial visualization of human blood basophils in autoradiographic preparations. Consecutive administration of 5-aminoacridine hydrochloride and aldehyde fuchsin rendered a sufficient preservation of basophils preventing leaching of their water soluble granules. Extensive control tests provided sufficient evidence to exclude chemographic artifacts produced by other histochemical precedures. The technique eliminates the obstacles to study the kinetics of human blood basophils and their realtionshp to atopic hypersensitivity reactions applying tritiated thymidine and radioiodine labeled IgE or corresponding antisera.

Acridines↗
PubMed1986

Heterogeneity of calcium channels in mast cells and basophils and the possible relevance to pathophysiology of lung diseases: a review.

Calcium plays a critical role in the formation and secretion of a wide variety of chemical mediators. Calcium slow-channel blockers, e.g. nifedipine and verapamil, have been shown to inhibit the synthesis of SRS (SRS-A, leukotrienes) in human and guinea pig lung tissue, thromboxane A2 formation in rat lung and platelet activating factor in human neutrophils. Verapamil and nifedipine also prevent the release of lysosomal enzymes from rabbit and human polymorphonuclear neutrophils. Calcium-channel blockers produce variable inhibitory effects on allergic and nonallergic histamine secretion. Ca++-entry blockers also inhibit the Ca++ uptake (influx) into mast cells. Many of these inhibitory effects of Ca++ antagonists are antagonized by an increased extracellular Ca++ ion concentration. The magnitude of the inhibitory influences of Ca++-channel blockers on allergic and nonallergic release of chemical mediators appears to depend on the cell source, species, nature and the concentration of the secretory stimuli as well as on the composition and pH of buffers and the concentration of Ca++-entry blockers used. The data summarized in this review suggest the existence of a functional heterogeneity of Ca++ channels in leukocytes, mast cells and basophils. Interference with the Ca++-dependent steps involved in the formation and/or release of chemical mediators appears to be the primary mode of action for Ca++-channel blockers in these cells. The differential effects of Ca++ antagonists on Ca++-dependent activation of phospholipase A2,5-lipoxygenase, and calmodulin (or other intracellular Ca++-binding proteins) in different cell types (mast cells, basophils, leukocytes, lung tissue, etc.) may explain the variation of their effectiveness in inhibiting the synthesis/release of chemical mediators and antagonizing bronchoconstriction in response to diverse stimuli. During the process of hypersensitization and in immediate hypersensitivity diseases, Ca++ homeostasis (uptake, mobilization, distribution, relocation, etc.) may be altered in leukocytes (mast cells, basophils) and lung tissues. The altered Ca++ homeostasis could be responsible for the induction of airway hyperreactivity in asthmatics and for hyperreleasability of chemical mediators from leukocytes, mast cells and other cell types.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Study of the effect of some neuropeptides and endogenous opioid peptides on in vitro histamine release from human lung mast cells and peripheral blood basophils.

In the present study we investigated the effect of substance P, bombesin, beta lipotropin, alpha and gamma endorphins, and metionin and leucin enkephalins on in vitro histamine release from partially purified human lung mast cells and peripheral blood basophils. In the concentration range of 10-100 microM, these neuropeptides and endogenous opioid peptides neither elicited a significant histamine secretions from human lung mast cells and blood basophils, nor influenced the anti-IgE-induced histamine release. These data indicate that human lung mast cells and blood basophils are resistant to the activity of substance P, bombesin, beta lipotropin, alpha and gamma endorphins, and metionin and leucin enkephalins, and confirm the functional heterogeneity of mast cells, depending on the species and the tissue origin.

Antibodies, Anti-Idiotypic↗
PubMed1986

Modulation of the release of histamine and arachidonic acid metabolites from human basophils and mast cells by auranofin.

In these experiments the effects of pharmacological concentrations of auranofin, a new absorbable gold compound, were assessed on the release of histamine and peptide leukotriene C4 (LTC4) from human basophils and lung mast cells. Auranofin, at pharmacological concentrations, inhibited in vitro histamine and LTC4 release from human basophils induced by anti-IgE. Inhibition began at about 3 X 10(-7) M and was maximum at 10(-5) M. We also evaluated the effect of auranofin on the release of histamine and LTC4 induced by anti-IgE from mast cells purified from human lung. Auranofin (3 X 10(-7) to 10(-5) M) dose-dependently inhibited the release of histamine and LTC4 from human lung mast cells. Thus pharmacological concentrations of auranofin cause dose-related inhibition of histamine release and de novo synthesis of LTC4 by human basophils and lung mast cells.

Adult↗
PubMed1981

A modulation of the anaphylactic basophil histamine release by selective H2 histamine agonists.

Two selective H2-histamine agonists, dimaprit and impromidine, have been tested for their action on histamine release from human basophils and rat mast cells. IgE-mediated basophil histamine release was inhibited by stimulation of histamine H2-receptors. However, differences between the actions of both dimaprit and impromidine were noticed. Both impromidine and dimaprit had no specific effect on 48/80-induced histamine release from rat mast cells, although the latter in higher concentrations either slightly increased spontaneous histamine release or non-specifically inhibited compound 48/80-induced release. The results are consistent with the view that activation of adenylate cyclase via H2-histamine receptors might be an important regulatory mechanism of histamine release from human basophils but not from rat mast cells.

Allergens↗
PubMed1981

Influence of preseasonal treatment with L-tyrosine-adsorbed allergoids on IgE-mediated histamine release from basophils of children suffering from allergic diseases.

In 10 children suffering from allergic pollinosis and/or asthma, a preseasonal hyposensitization scheme with 3 weekly injections of a glutaraldehyde-modified, tyrosine-adsorbed grass-pollen allergen reduced the histamine release from basophils in response to increasing concentrations of antigen. The decrease in histamine release which occurred 1 week after the injection course was even maintained during the pollen season. The inhibition was only obtained when basophils were incubated with the serum of patients, but not with the serum of normals, indicating that blocking antibodies may have occurred. In contrast to what has been observed in the treated patients' group, 5 patients, who were not included in the hyposensitization scheme, showed identical histamine release curves during the whole investigation period. Specific IgE did not increase after the treatment course and shows the same behaviour as the untreated patients. Thus, as treatment with glutaraldehyde modified, tyrosine-adsorbed allergoids is safe to administer, requires only 3 injections, reduces histamine release from basophils by production of "blocking" antibodies, it appears to be a useful tool in the hyposensitization treatment.

Adsorption↗
PubMed1994

Control function of protein kinase C isozymes on leukotriene generation from human basophils?

Arachidonic acid metabolites generated from activated basophils and/or mast cells mediate different types of cutaneous inflammatory reactions. To clarify the mechanisms of leukotriene C4 (LTC4) production from human basophils, cells were purified from the peripheral blood by negative selection with immunobeads. The protein kinase C (PKC) activators 12-O-tetradecanoyl-phorbol-13-acetate, phorbol-12,13-dibutyrate and phorbol-12,13-didecanoate did not induce a significant LTC4 generation from human basophils in vitro, indicating that phorbol-ester-sensitive PKC isozymes are not involved in the mechanisms of arachidonic acid metabolism in these cells. However, selective PKC inhibitors (Ro 31-7549, ilmofosine, GF109203X, and calphostin C) potentiated the IgE-mediated LTC4 production in a dose-dependent fashion. We therefore suggest that PKC isozymes which are influenced by these inhibitors modulate the degree of LTC4 release after stimulation with anti-IgE antibodies.

Basophils↗
PubMed1982

Fine structures of the basophil infiltration in regional lymph nodes of the guinea-pig after the intradermal injection of T cell mitogens.

Basophil-rich infiltrates in regional lymph nodes of guinea-pigs were demonstrated by electron microscopy after the intradermal injection of T cell mitogens (PHA and Con A). Basophils infiltrated the stroma of the lymph node via the postcapillary venules (PCV) and migrated to the paracortex. Prior to infiltration of the lymph nodes a cutaneous basophil hypersensitivity reaction was seen in the mitogen-injected skin. B cell mitogen (LPS) injection did not induce this response.

Animals↗
PubMed1998

Immunopharmacology of human mast cells and basophils.

Human mast cells and basophils play a key role in the pathogenesis of several immunological and inflammatory disorders, not only by producing inflammatory and fibrogenic mediators, but also by directly (CD40 ligand) and indirectly secreting various cytokines and chemokines. Studies carried out to evaluate the effects of drugs that modulate the release of mediators and cytokines from these cells have contributed to clarifying the biochemical mechanism by which immunological and non-immunological stimuli activate these cells. Significant differences have been documented between human mast cells and basophils as regard the pharmacological agents that modulate the release of mediators, between mast cells isolated from different anatomical sites, and between compounds of the same class of drugs. Efforts to gain insight into the biochemical events occurring during immunological activation of mast cells and basophils could lead to the identification of new biochemical targets for therapeutic interventions in several immunological disorders.

Adenylyl Cyclases↗
PubMed2002

Basophils in airway disease.

The inflammatory response that is often associated with asthma is characterized by the recruitment of eosinophils, basophils, and lymphocytes. Until recently, profiling the basophil and defining its functional characteristics have been difficult. With the advent of some new tools, there is a steadily increasing body of information on the presence and potential activities of the basophil. Although the precise role of these cells in airway diseases, such as asthma, remain unclear, relatively accurate enumeration is now possible. Coupled with new insights into cytokine secretion from these cells, a more accurate picture of the dynamics of this specialized form of inflammation is available for refining our hypotheses regarding its regulation.

Basophils↗
PubMed2005

Basophils and mast cells in chronic idiopathic urticaria.

Chronic idiopathic urticaria (CIU) is diagnosed in patients when urticarial eruptions recur for more than 6 weeks, and no specific cause is determined. Given that urticaria resembles the lesions induced by injection of histamine or allergen into the skin, a role for mast cells or basophils has been proposed in the generation of localized urticarial lesions. However, currently, the exact mechanisms governing regional mast cell or basophil activation are unknown. In the past decade, there has been mounting interest in viewing CIU as an autoimmune disease, given the presence of circulating autoantibodies to IgE or the alpha subunit of the high-affinity IgE receptor (FceRI) in a subset of patients. In this review, we propose that in addition to autoantibodies, specific differences in the expression of FceRI-signaling molecules in the basophils or mast cells of CIU patients may contribute to the generation of urticarial eruptions.

Autoantibodies↗