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At least 1,081 records · Page 60Linked to original sources
PubMed1988

Human C5a induces a substantial histamine release in human basophils but not in tissue mast cells.

The histamine-releasing effect of human C5a was compared with that of concanavalin A in blood basophils and isolated adenoidal mast cells from the same donors. In basophils, C5a (10 ng/ml) induced a significant histamine release (7.5 +/- 2.1%, corrected value). In isolated adenoidal mast cells C5a had only a marginal effect (2% histamine release), although the cells responded markedly to concanavalin A stimulation (about 13% release). The results support the view that the heterogeneity of mast cells and basophils is also reflected in the expression of anaphylatoxin receptors on their surface.

Adenoids↗
PubMed1988

Release of highly-sulphated glycosaminoglycans and histamine from human basophils.

A new assay for highly-sulphated glycosaminoglycans (GAGs) has been applied to the study of allergen (Dermatophagoides pteronyssinus)-induced release of GAG from human basophils. Highly-sulphated GAG, which was not heparin, was found only in basophil-containing cellular fractions of whole blood. Its release, like that of histamine, was Ca++-dependent. However, allergen-induced release of GAG from the basophils of atopic individuals exhibited a different time-course and dose-response from that of histamine, and may occur at least in part by a different mechanism.

Adult↗
PubMed1990

Basophil releasability in human hydatidosis.

We studied immunoglobulin E (IgE)- and non-IgE-mediated releasability in basophils from 31 patients with hydatidosis. Histamine release to non-IgE-dependent stimuli did not differ significantly between normal individuals and patients with hydatidosis. On the contrary, an increased histamine liberation was obtained by challenging basophils from hydatid patients with anti-human IgE. It is concluded that Echinococcus granulosus infection induces an enhanced sensitivity of basophils to IgE-dependent stimuli.

Animals↗
PubMed1990

Sequential appearance of basophils and mast cells from human bone marrow in long-term suspension culture.

Human bone marrow cells grown in liquid culture in the presence of conditioned medium from concanavalin A stimulated peripheral blood mononuclear cells, from mixed lymphocyte reactions, or from an osteogenic sarcoma tumor line gave rise to basophils which were maximal in number at 1-3 weeks. Basophils had a multilobed nucleus, contained large cytoplasmic granules of variable size which stained metachromatically with acid, but not neutral toluidine blue, were negative for chloroacetate esterase, and did not contain human mast cell tryptase. In long-term cultures, mast cells were detected after 5-6 weeks. Mast cells had cytoplasmic granules that stained with acid and neutral toluidine blue, were positive for chloroacetate esterase, and contained human mast cell tryptase. It, therefore, appears that in liquid cultures even in the absence of feeder layers, human bone marrow cell cultures can give rise initially to basophils, and then to mast cells.

Animals↗
PubMed1992

Effects of anti-CD11a, anti-CD11b and anti-CD18 on histamine release from human basophils primed with IL-3.

This study was carried out to investigate the possible role of adhesion molecules in the histamine release from human basophils primed with recombinant IL-3 (rIL-3). Anti-IgE monoclonal antibody (0.1 microgram/ml) did not induce apparent histamine release by itself, however, remarkable histamine release was induced from rIL-3-primed human basophils triggered by anti-IgE. Bear-1 (anti-CD11b monoclonal antibody) inhibited the histamine release enhanced by rIL-3, however SPV-L7 (anti-CD11a monoclonal antibody) or CLB-LFA1/1 (anti-CD18 monoclonal antibody) did not inhibit the histamine release enhanced by rIL-3 at all. The present study suggests that alpha-chain of Mac-1 is involved in the priming effect of IL-3 to increase histamine release from human basophils.

Antibodies, Monoclonal↗
PubMed1992

Pharmacological studies on the role of protein kinase C in signal transduction of human basophils.

Recent investigations have demonstrated that activation of basophils involves the activation of protein kinase C (PKC). In the present study the effects of different nonselective and selective PKC inhibitors on IgE-mediated histamine release from human basophils were investigated. While potent but nonselective inhibitors such as staurosporine exerted a dose-dependent inhibition of Fc epsilon-receptor-mediated histamine release, staurosporine derivatives with high selectivity for PKC potentiated the IgE-mediated response. The results provide evidence that the histamine release-inhibiting activity of protein kinase inhibitors is inversely correlated with their specificity for PKC. This may confirm the hypothesis that PKC exerts a negative modulatory role during the process of stimulus secretion-coupling following receptor aggregation in basophils. Moreover, investigations with phorbol esters and diacylglycerol derivatives as potent PKC activators show that direct cellular PKC activation and antigen-stimulated mediator release are not closely correlated.

Basophils↗
PubMed1993

Pharmacologic control of histamine release from human basophils induced by platelet-activating factor.

We studied the effect of several compounds that influence different cell activation steps on platelet-activating factor (PAF)-induced basophil histamine secretion. Isobutylmethylxanthine (1-100 microM), dimaprit (1-100 microM) and dibutyryl adenosine 3',5'-cyclic phosphate (cAMP; 0.01-1 mM), that increase intracellular cAMP levels, concentration-dependently inhibited PAF-elicited histamine release. Rolipram (phosphodiesterase, PDE, isotype IV inhibitor; 0.1 nM-10 microM) potently inhibited histamine secretion activated by PAF, whereas SKF95654 (PDE III inhibitor; 0.01-10 microM) was ineffective. The kinase inhibitor, staurosporine (0.1-100 nM), enhanced PAF-induced basophil histamine release, whereas the G-protein inhibitor, pertussis toxin (1 microgram/ml), had an inhibitory effect. The specific lipoxygenase inhibitor, AA-861 (0.1-10 microM), inhibited PAF-activated histamine release, while the leukotriene A4 hydrolase inhibitor, bestatin (100 microM), had only a marginal effect. Finally, the Ca2+ channel entry blockers, verapamil (3-30 microM) and zinc (1.5-50 microM), inhibited PAF-induced histamine release. These results suggest that PAF is a unique secretagogue for human basophils unlike antigen, anti-IgE or univalent stimuli.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Inhibitory effect of the H1 antagonist loratadine on histamine release from human basophils.

Loratadine is a powerful H1 antagonist commonly employed in the treatment of allergic disorders. The present study was performed to investigate whether loratadine, in addition to anti-H1 activity, is able to modulate histamine release from human basophils. Leukocyte suspensions were prepared by dextran sedimentation of peripheral venous blood drawn from 10 normal subjects. Leukocytes were stimulated with anti-IgE (1/5,000), N-formyl-methionyl-leucyl-phenylalanine (FMLP; 10 microM) and the Ca2+ ionophore A23187 (1 microM), and histamine release in the cell supernatants was measured by an automated fluorometric method. Loratadine, at concentrations ranging from 1 to 50 microM, exerted a dose-dependent inhibitory effect on IgE-mediated and IgE-independent histamine release. The concentrations inhibiting 50% of histamine release were 30 microM (anti-IgE), 29 microM (FMLP) and 24 microM (Ca2+ ionophore A23187). The inhibitory activity of loratadine was optimal after incubation for 2 h at 37 degrees C and the effect of the drug was no longer evident when leukocytes were stimulated 2 h after cell washing. Increased extracellular Ca2+ concentrations reduced the inhibitory activity of loratadine, indicating that external Ca2+ and loratadine have antagonistic effects on basophil histamine release. These results indicate that loratadine, in addition to H1 receptor blocking activity, has the capacity to inhibit histamine release from human basophils.

Adult↗
PubMedDate not supplied

Basophil and eosinophil activation by CC chemokines.

Recent studies have shown that CC chemokines act on monocytes, lymphocytes, eosinophils and basophils, but not neutrophils, with distinct target cell selectivities, possibly explaining the selective attraction and activation of these cell types in different types of chronic inflammation and allergic disease. Functional and desensitization studies on basophils and eosinophils indicate the expression of at least three distinct G-protein-coupled CC chemokine receptors (three on basophils and two on eosinophils), which exert partially selective and partially overlapping ligand specificities and also appear to mediate distinct functions despite similar signal transduction pathways. Functional studies with all known six human CC chemokines show that each cytokine has a distinct spectrum of bioactivities and target cell profile. Interestingly, overall sequence homologies between the chemokines are not predictive for the cell function or cell type that a particular chemokine will preferentially activate, and thus discrete sequence motifs may be important for activating the different CC chemokine receptors. Using different chemokine mutants and hybrids between chemokines, the functional importance of selected individual amino acids and short motifs are now being analysed. These structure-function studies could also lead to antagonists that have more disease-selective anti-inflammatory properties than currently available drugs.

Basophils↗
PubMed1995

Effect of CC chemokines on mediator release from human skin mast cells and basophils.

Chemokines are considered important mediators of various inflammatory processes. In human basophils, different CC chemokines are known to stimulate release of histamine and generation of leukotriene (LT)C4. In the present study, we have evaluated the effect of RANTES (regulated upon activation, normal T cell expressed and secreted), monocyte chemotactic protein (MCP)-1, MCP-2, MCP-3, macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta on mast cell activation. Whereas all these CC chemokines caused dose-dependent release of histamine from basophils in mixed human leukocyte suspensions, none of them was able to induce release of histamine as well as tryptase or prostaglandin (PG)D2 from human skin mast cells, nor did priming with these substances enhance IgE-mediated mediator release. In addition, all chemokines failed to promote changes in the cytosolic free calcium level in the human mast cell line HMC-1. These results add further evidence for the differences between human mast cells and basophils regarding cytokine-dependent activation.

Basophils↗
PubMed1996

Immunophenotypic analysis of HL-60 cells during basophilic differentiation.

Differentiation along specific myeloid lineages may be accompanied by characteristic cell surface marker changes. We have examined leukemic HL-60 cell changes under conditions which induce basophilic differentiation. An increased surface expression of CD35, CD11b, and decreased expression of CD15 was found by flow cytometry during the 5-day induction period. Further investigation revealed two cell populations after 5 days in vitro: (i) a CD35-positive population (61% of cells present) containing a significant number of CD15-negative cells, and (ii) a CD15-positive/CD35-negative population. The CD35-positive subset appears to account for the majority of the basophilic cells induced under these conditions, as measured by histamine content and metachromatic staining. In addition, this subset contains a small number of early monocytic cells (CD14 and CD23 positive). The expression of CD11b is variably found on the CD15-positive/ CD35-negative subset of induced cells. These results suggest that CD35 and CD15 surface immunophenotyping can be used to map steps involved in myeloid development. A role for CD35 and CD15 in early basophil differentiation is proposed.

Antigens, CD↗
PubMed1996

Oxatomide inhibits the release of proinflammatory mediators from human basophils and mast cells.

Oxatomide (OXA), a histamine H1 receptor antagonist, is effective in the treatment of patients with allergic rhinitis, some allergic skin disorders, and bronchial asthma. We have characterized the effect of OXA on the immunologic release of preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4:LTC4 and prostaglandin D2:PGD2) from human basophils and mast cells purified (from 10 to 82%) from human lung parenchyma (HLMC) and skin tissue (HSMC). Preincubation (15 min, 37 degrees C) of basophils with OXA (10(-7)-10(-5) M) before Der p I antigen or anti-IgE challenge concentration-dependently (10-40%) inhibited the immunologic release of histamine and LTC4. OXA (10(-7)-10(-5) M) also inhibited (10-40%) histamine, tryptase and LTC4 release from HLMC activated by anti-IgE. In addition, OXA caused a concentration-dependent inhibition of histamine, tryptase and PGD2 release from HSMC immunologically challenged with a monoclonal antibody against the alpha chain of the high affinity receptor for IgE (anti-Fc epsilon RI) or anti-IgE. These results demonstrate that OXA exerts anti-inflammatory activities by inhibiting the release of preformed and de novo synthesized mediators from human basophils and mast cells.

Adult↗
PubMed1993

Influence of protein kinase C activation on basophils from patients with atopic dermatitis in comparison with nonatopic controls.

Protein kinase C (PKC) is suggested to be important for signal transduction of histamine-containing cells. The present study investigated the putative role of PKC in enhanced mediator release of basophils in atopic dermatitis (AD). Basophils were isolated from patients with severe AD (mean serum IgE level of 5,165 U/ml) and from healthy controls, and the effects of potent activators of PKC on histamine release were studied. The phorbol esters 12-o-tetradecanoyl-phorbol-13-acetate and phorbol-12,13-dibutyrate and the nonphorbol mezerein induced a dose-dependent mediator release, which was significantly lower in 'atopic' basophils at concentrations > or = 1 microM. Recently, PKC levels have been shown to be lowered in atopic leukocytes compared to cells from healthy controls. The lowered response of PKC towards direct activation and lowered PKC levels may be due to high serum IgE levels and allergen exposure in vivo with subsequent down-regulation of different key elements of signal transduction.

Adolescent↗
PubMed1998

RANTES induces nasal mucosal inflammation rich in eosinophils, basophils, and lymphocytes in vivo.

RANTES is a CC chemokine that causes chemotaxis of eosinophils, basophils, and lymphocytes in vitro. The objective of this study was to investigate the effect of RANTES on the influx of inflammatory cells into the nasal mucosa of 12 allergic patients. In the first phase, each patient was challenged with RANTES or diluent on two subsequent days. RANTES caused a significant (p < 0.05) influx of eosinophils as compared with the diluent. The number of eosinophils were 5,548 +/- 1,532/ml and 462 +/- 206/ml after RANTES and diluent challenge, respectively, at the peak of the response at 2 h. There was also a significant influx of metachromatic cells and lymphocytes, but not monocytes, neutrophils, or epithelial cells after RANTES challenge. In the second phase, the patients were first challenged with an allergen and 24 h later, challenged with RANTES or diluent. In the allergen-primed mucosa RANTES induced a significantly higher influx of eosinophils, basophils, and lymphocytes. Further, RANTES caused migration of monocytes and neutrophils, and shedding of epithelial cells. The influx of the inflammatory cells was associated with symptoms of rhinitis. We conclude that RANTES induces a clinically symptomatic inflammatory response in vivo by causing chemotaxis of eosinophils, basophils, and mononuclear cells.

Adult↗
PubMed1990

Disassociation of the release of histamine and arachidonic acid metabolites from osmotically activated basophils and human lung mast cells.

Upon activation by most stimuli, basophils and human lung mast cells simultaneously release histamine and arachidonic acid metabolites. Hyperosmolar activation was examined, and both cell types were shown to release histamine but little or no leukotriene C4 or D4 (LTC4/D4) and, in the case of mast cells, little or no prostaglandin D2 (PGD2). In addition, hyperosmolar buffers were capable of preventing the formation of LTC4/LTD4 in basophils stimulated by anti-IgE when added simultaneously, or 2, 5, or 10 min after, the addition of anti-IgE. Catabolism of PGD2 and LTC4/D4 was not increased. Experiments with cell lysates demonstrated that intracellular formation, rather than secretion, was arrested in hyperosmolar buffers. We conclude that this selective inhibition of mediator production is a unique response of mast cells and basophils to osmotic activation. Although the mechanism of this selective cellular response is not clear, these in vitro observations have important therapeutic and pathophysiologic implications for the airway response to hyperosmolar stimuli.

Antibodies, Anti-Idiotypic↗
PubMed1980

Basophil "releasability" in patients with asthma.

This study was based on the premise that mediator release plays a role in the pathogenesis of allergen-induced as well as nonallergen-induced asthma. We studied histamine release from human basophils obtained from patients with asthma and from control subjects. These cells were challenged with several different stimuli: goat anti-human IgE-Fc, C5-peptide, N-formyl-methionyl-leucyl-phenylalanine (f-met peptide), Ca++ ionophore A23187, hyperosmolar mannitol, and D2O. Release induced by any one stimulus was unrelated to the response to any other stimulus. The basophils of patients with asthma and control subjects responded similarly to most stimuli: they were significantly less responsive to C5-peptide and f-met peptide, and significantly more responsive to D2O. The results suggest that there is a parameter of releasibility that must be defined for each separate stimulus, and that patients with asthma can be differentiated from normal persons by the response of their basophils to selected stimuli.

Adult↗
PubMed1979

Anaphylactic relase of a basophil kallikrein-like activity. II. A mediator of immediate hypersensitivity reactions.

This report describes the immune release of a new mediator from human peripheral leukocytes, a basophil kallikrein-like activity (BK-A). The release process is initiated by the interaction of antigen on anti-IgE with cell-bound IgE, and appears to be similar in mechanism to the relase of histamine and other mediators of the immediate hypersensitivity reaction. The dose-response relationships and kinetics of histamine and BK-A release from antigen-challenged peripheral leukocytes are similar. The relase of the BK-A is calcium and temperature dependent, requires metabolic energy, and is controlled by hormone-receptor interactions that influence the cellular level of cyclic AMP, as has been described for other mediators of immediate hypersensitivity reactions. The data indicate that the interaction of BK-A with human plasma kininogen, generates immunoreactive kinin. We conclude that the antigen-IgE interation leads to the release from human basophils of a new mediator, a basophil kallikrein-like activity which may well be a link between reactions of immediate hypersenstivitity and the plasma and/or tissue kinin-generating systems.

Anaphylaxis↗
PubMed1988

Differential effects of the complement peptides, C5a and C5a des Arg on human basophil and lung mast cell histamine release.

The ability of purified anaphylatoxins to induce human lung mast cell mediator release was investigated. In eight anti-IgE responsive (histamine release = 22 +/- 5%, mean +/- SEM) mast cell preparations of 1-96% purity, C5a and C5a des Arg (0.55 pg/ml to 55 micrograms/ml), failed to elicit or potentiate histamine release; lung fragments were similarly unresponsive. The related peptide C3a was also inactive. All anaphylatoxins failed to induce mast cell leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) release. LTC4 release was also negligible from basophils where C5a was a potent histamine release stimulus. Supernatants from C5a-challenged mast cells remained fully active on basophils, excluding carboxypeptidase inactivation of C5a as an explanation for the lung mast cell results. In contrast to lung, skin mast cells were C5a-responsive (histamine release = 8 +/- 1%, at 55 micrograms/ml, n = 2). We conclude that C5a, though devoid of activity on the human lung mast cell, is a human basophil and skin mast cell secretagogue. These findings demonstrate significant organ-specific heterogeneity in mast cell responsiveness.

Basophils↗