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At least 649 records · Page 36Linked to original sources
PubMed2006

Comparison of basophil activation tests using CD63 or CD203c expression in patients with insect venom allergy.

BACKGROUND: Flow cytometric basophil activation tests have been developed as cellular tests for in vitro diagnosis of IgE-mediated reactions. Different activation markers (CD63 or CD203c) with distinct ways of regulation have been used after stimulation with various allergens. OBJECTIVE: It was the aim of the present study to compare basophil activation tests by measuring both CD63 and CD203c upregulation in patients with insect venom allergy. MATERIALS AND METHODS: 43 patients with a history of insect venom anaphylaxis were examined. A careful allergy history was taken, and skin tests and determination of specific IgE-antibodies were performed. Basophil activation tests (BAT) using CD63 or CD203c expression were done after stimulation with different concentrations of bee and wasp venom extracts. 25 healthy subjects with negative history of insect venom allergy were studied as controls. RESULTS: The CD203c protocol showed a slightly higher sensitivity than the CD63 protocol (97% vs. 89%) with regard to patients' history. The magnitude of basophil response was higher with CD203c in comparison to CD63 for both insect venoms. Specificity was 100% for the CD63 protocol and 89% for the CD203c protocol with regard to controls with negative history and negative RAST. CONCLUSION: These results support the reliability of basophil activation tests using either CD63 or CD203c as cellular tests in the in vitro diagnosis of patients with bee or wasp venom allergy with a slightly higher sensitivity for the CD203c protocol.

Allergens↗
PubMed1996

Histamine releasing cells of the newborn. Mast cells from the umbilical cord matrix and basophils from cord blood.

The cellular branch of the immune defence in the newborn has been shown to differ from adults in a number of ways. This report presents new data on the functions of the histamine-secreting cells of the newborn. Mast cells of the newborn were obtained from the human umbilical cord by enzymatic dispersion. The granules of the mast cells of the umbilical cord were found to contain both chymase and tryptase by immunohistochemical staining, and the presence of cell-bound IgE on the mast cell surface was demonstrated by staining sections of umbilical cord with peroxidase-conjugated anti-IgE. The enzymatic dispersion yielded 12,660 mast cells per gram umbilical cord (median), range 2,500-60,300 (n = 48). The mast cells were found to constitute 3.1% of the total nucleated cells in the dispersate (median), range 1.5-3.8%. The histamine release from these cells was measured using a glass microfibre-based method. Both the umbilical cord mast cells and the cord blood basophils released histamine stimulated with anti-IgE, concanavalin A and the calcium ionophore A23187. In contrast to mast cells from adult tissue, the phorbol ester TPA was found to be an efficient secretagogue in both mast cells and basophils from the newborn. After maximal stimulation with anti-IgE and phorbol ester the quantity of histamine released per millilitre of blood was significantly higher in cord blood than in adult blood. The spontaneous histamine release from cord blood basophils was also significantly higher than from adult blood basophils. The mast cells found in the umbilical cord matrix and the cord blood basophils represent a readily available source of metabolically active histamine releasing cells for exploration of the role of histamine-secreting cells in newborn immune defence.

Adult↗
PubMed1990

Allergy testing using degranulation of basophils and flow cytometry.

The Technicon H6000 hematology system was evaluated as a detector for the allergen-induced basophil degranulation reaction in whole blood samples from individuals with type I allergy. Diluted standard skin prick test allergen extracts were added into heparin-EDTA blood samples in presence and absence of free calcium ions and the H6000 basophil channel scattergram was used with a modification of the method for basophil counting. In one experiment only 250 microliters of blood was used for each allergen to be tested. The result correlated well to skin prick test and RAST results. The conclusions are that the H6000 is suitable for allergy testing using whole blood from patients, if the basophil channel is modified, and that the Technicon H1 system probably also is possible to use as a detector for basophil degranulation studies.

Allergens↗
PubMed1991

The role of basophils in asthma.

The characteristics of the acute and late human response to antigen in the upper and lower airways and in the skin is summarized in TABLE 2. This table makes it clear that while mast cells are responsible for the mediator release of the acute phase, eosinophils and basophils are the cells involved in the mediator release which occurs during the experimental late phase reaction. The pattern of mediators observed during the acute response is quite characteristic of the mast cell. Thus, in the nose, skin, and lungs, the acute response is characterized by significant increases in histamine, PGD2, tryptase, and sometimes LTC4. In the late phase reaction, the pattern of mediator release is characteristic of basophils and eosinophils, and includes histamine, LTC4 (where measurable), and eosinophil-derived proteins, without PGD2 or tryptase. Basophils have been identified at appropriate time-points in each model using morphologic and phenotypic criteria, and their numbers relate to the histamine levels. Finally, treatment with glucocorticosteroids, the most potent drugs available for treating chronic allergic inflammation, obliterates the late phase reaction and decreases both mediator release and the infiltration of eosinophils and basophils. Chronic allergic inflammation is now taken by both the pulmonary and immunologic community as a hallmark of asthma, and it can be stated without equivocation that the basophils are responsible for the mediator release observed in that response.

Asthma↗
PubMed2001

Basophils and exercise-induced hypoxemia in extreme athletes.

This study examined whether the increase in histamine release (%H, i.e., plasma histamine expressed as a percentage of whole blood histamine) associated with exercise-induced hypoxemia (EIH) is related to high training-induced changes in basophil and osmolarity factors in arterial blood. All parameters were measured in 20 endurance athletes, 11 of whom presented an EIH (HT(hyp)) and 9 of whom were nonhypoxemic (HT(nor)), and in 10 untrained control subjects (UT). Measurements were made at rest, at the maximal workload of an incremental exhaustive exercise test, and at the fifth minute of recovery. %H increased during exercise in HT(hyp) (P < 0.01) but did not increase significantly in HT(nor) and UT controls. The results indicated that 1) osmolarity and Na(+) and K(+) concentrations did not differ between the two trained groups and 2) the basophil count and basophil histamine content did not differ among groups. We concluded that the %H increase associated with EIH was not due to a training effect on these parameters. The relatively low increase in histamine content during exercise in HT(hyp) in comparison to HT(nor) (P < 0.05) and UT (P < 0.01) and the low recovery vs. resting basophil count only in HT(hyp) (P < 0.01) suggested an accentuated exercise-induced basophil degranulation in the hypoxemic athletes.

Adult↗
PubMed2004

The basophil-specific ectoenzyme E-NPP3 (CD203c) as a marker for cell activation and allergy diagnosis.

Basophils are effector cells of allergic reactions. These cells produce and store a number of vasoactive and immunomodulatory mediators. During an allergic reaction, basophils can release their mediator substances into the extracellular space and thus contribute to the clinical picture and symptoms in allergy. The phenotypic hallmark of basophils is expression of high-affinity IgE receptors (Fc epsilon RI) on their cell surface together with expression of the activation-linked molecule CD203c. This ectoenzyme is located both on the plasma membrane and in the cytoplasmic compartment of basophils. Cross-linking of the Fc epsilon RI by an allergen or anti-IgE antibody results in a rapid upregulation of intracellular CD203c molecules to the cell surface and is accompanied by mediator release. CD203c is therefore a promising target molecule for a flow cytometry-based test to analyze sensitized individuals and patients with type I allergy. In the present article, we review the current knowledge of CD203c with special regard to its tissue distribution and regulation in basophil activation. In addition, we discuss the application of CD203c in allergy diagnosis.

Animals↗
PubMed2004

Expression of actin and tubulins in purified human basophil leukocytes upon stimulation with IL-3.

BACKGROUND: Pharmacological and morphological results indicate that the cytoskeleton proteins tubulins and actin play a role in the histamine release process in basophil leukocytes and mast cells. In this report, we investigate the expression of these cytoskeleton proteins in purified human basophils upon stimulation with anti-IgE and IL-3. METHODS: Human basophils were purified using a negative selection procedure. They were incubated for 6 h with anti-IgE and/or IL-3 in radiolabeling media. Proteins in the cells were analyzed by two-dimensional gel electrophoresis and autoradiography. Actin and alpha- and beta-tubulin were identified by amino acid sequence analysis or matrix assisted laser desorption/ionisation time-of-flight mass spectrometry. The synthesis of these proteins under different experimental conditions was evaluated by densitometry. RESULTS: Actin is regulated dose dependently by IL-3 with an optimum concentration of 100 ng/ml, corresponding to the optimal IL-3 concentration for enhancement of histamine release. The synthesis of tubulins was not significantly upregulated by IL-3 or anti-IgE alone, but there was a slight and significant upregulation of tubulins upon stimulation with both IL-3 and anti-IgE in doses optimal for maximal histamine release. CONCLUSIONS: The de novo synthesis of actin is regulated dose dependently by IL-3 in purified human basophils in short-term culture. The optimum IL-3 concentration is the same as for enhancement of histamine release, suggesting that the same processes that regulate IL-3-induced enhancement of histamine release also regulate the expression of actin. The finding that the expression of the tubulins is not upregulated by IL-3 alone suggests that regulation of tubulin synthesis is not a pathway by which IL-3 in itself primes basophil histamine release.

Actins↗
PubMed2006

Luteolin, a flavonoid, inhibits CD40 ligand expression by activated human basophils.

BACKGROUND: We have previously shown that flavonoids such as luteolin, apigenin and fisetin inhibit interleukin 4 and interleukin 13 production. In this study, we investigated whether luteolin can suppress CD40 ligand expression by basophils. METHODS: A human basophilic cell line, KU812, was stimulated with A23187 and phorbol myristate acetate (PMA) with or without various concentrations of luteolin or other flavonoids for 12 h, and CD40 ligand expression was analyzed by FACS. The effect of luteolin on CD40 ligand mRNA expression was studied by semiquantitative reverse transcription PCR analysis. In addition, CD40 ligand expression was also measured in purified basophils that had been stimulated for 12 h with A23187 plus PMA with or without various concentrations of luteolin. RESULTS: CD40 ligand expression by KU812 cells was enhanced noticeably in response to A23187 and even more strikingly augmented by A23187 plus PMA. The expression was significantly suppressed by 10 or 30 microM of luteolin, whereas myricetin failed to inhibit. Reverse transcription PCR analyses demonstrated that luteolin inhibited CD40 ligand mRNA expression by stimulated KU812 cells. Of the six flavonoids examined, luteolin, apigenin, fisetin and quercetin at 30 microM showed a significant inhibitory effect on CD40 ligand expression. The incubation of purified basophils with A23187 plus PMA significantly enhanced CD40 ligand expression, and the presence of luteolin again had an inhibitory effect. CONCLUSIONS: Luteolin inhibits CD40 ligand expression by activated basophils.

Apigenin↗
PubMed1977

Quantitation of basophil-bound IgE in atopic and nonatopic subjects.

Basophil-bound IgE was measured by quantitative immunofluorescence microscopy in atopic subjects and in healthy controls. A correlation was found between IgE serum level and basophil-bound IgE. The basophils from the atopic patients, both from those with a low and those with an increased serum IgE, showed a significantly higher fluorescence intensity than the basophils from the respective controls. Our results indicate that both atopy and the IgE level of the serum determine the amount of basophil-bound IgE.

Adolescent↗
PubMed1984

Transmethylation reactions in human basophils induced by anti-IgE or specific antigen.

The activation of methyl transferases in the membrane of human basophilic leukocytes was measured by incorporation of 3H-methyl groups into phospholipids. Basophils of healthy individuals were activated by anti-IgE, those of pollen allergic patients by the specific antigen, Lolium perenne extract. Basophil-rich fraction was obtained from peripheral blood by centrifugation in a gradient of Ficoll/metrizamide (g = 1.085). After incubation with anti-IgE an increase in the 3H-methyl incorporation was detected during the first 30 s of the reaction. The maximal incorporation in basophils of the pollen allergic patients, activated by L. perenne extract, was enhanced at 15 s. Appropriate controls showed that the activation of methyl transferases occurred in basophils only.

Animals↗
PubMed1990

Modulation of rat peritoneal mast cell and human basophil histamine release by estrogens.

This study was undertaken to investigate the effect of estrogens on the histamine release mediated by IgE in rat peritoneal mast cells (PMC) and in sensitized human basophils. The estrogens were found to enhance the histamine release of either rat PMC and sensitized human basophils upon stimulation with anti-IgE. The enhancement was estrogens dose-dependent reaching the maximum value of 23% for rat PMC and 41% for sensitized human basophils stimulated with anti-IgE upon preincubation with 10(-8) M estrogens. Moreover, when purified PMC were used, the enhancing effect was still detected, suggesting a direct interaction between estrogens and mast cells. The enhancing effect took place quite rapidly reaching plateau levels in about 60 min. Basophils preincubated at 4 instead of 37 degrees C did not give any appreciable enhancement, suggesting that it was temperature-dependent and that the effect observed was not due to cytotoxicity. Incubation of PMC or human basophils with estrogens alone, without challenge with anti-IgE, did not give any detectable histamine release. The enhancement of histamine release by estrogens is probably mediated by IgE molecules present on the cell membrane, since this effect was not observed on challenge with substance P or compound 48/80, two segretagogues known to induce histamine release not via IgE.

Animals↗
PubMed1993

Purification of normal human bone-marrow-derived basophils.

It is well established that basophils and eosinophils share a common differentiation pathway, although the factors regulating their terminal commitment (towards one or other lineage) are not yet fully defined. Interleukin-3 (IL-3) is a major differentiation factor for both human eosinophils and basophils, yielding a mixed population composed predominantly of eosinophilic cells (65 +/- 9%; n = 4), basophils at different stages of maturity (29 +/- 6%; n = 4) and monocytes/macrophages (6 +/- 3%; n = 4), after 3-4 weeks in culture. Using a relatively rapid and simple method involving a first step of gradient density centrifugation over a Percoll gradient (d = 1.063 g/ml) and a subsequent step of adhesion on tissue-culture-treated plastic, a cell population composed of 94 +/- 5% normal basophils and their precursors, with no demonstrable mast cells, was reproducibly obtained from human hematopoietic cells cultured for 3-4 weeks in the presence of recombinant IL-3. These cells contained high levels of histamine (1.39 +/- 0.14 pg/cell) and released this mediator upon stimulation with calcium ionophore A23187 and in a dose dependent manner upon stimulation with IgE-anti IgE, demonstrating their functional capacity. This relatively simple method therefore permits the production of large quantities of pure populations of normal and functional human bone-marrow-derived-basophils.

Basophils↗
PubMed1994

Antibodies specific to membrane components of rat mast cells are cross-reacting with human basophils.

Murine monoclonal antibodies (mAbs) have previously been raised by us with specificity to the following plasma membrane components of rat mucosal mast cells (RBL-2H3 subline): (1) the alpha-subunit of the type I Fc epsilon receptor, (Fc epsilon RI); (2) a newly described membrane glycoprotein, distinct from any of the Fc epsilon RI subunits, yet affecting the cell's secretory response to Fc epsilon RI clustering and hence named mast cell functional antigen (MAFA), and (3) a glycolipid, GD1b present in the RBL-2H3 cell's plasma membrane. The cross-reactivity of these mAbs with human basophils (from both allergic and nonallergic children) was now examined by three different protocols: (1) by microscopy (light and dark field) of double stained basophils by toluidine blue and by fluorescein-labeled anti-mouse antibodies as secondary ligands binding to the mAbs; (2) by flow cytometry (using directly labeled mAbs), and (3) by monitoring the binding of the 125I-radiolabeled mAbs. In order to exclude the possibility of the (intact) mAbs binding to the Fc gamma receptors, also present on human basophils, Fab and (Fab')2 fragments derived from the above respective mAbs were employed wherever necessary. The results show that the above described murine mAbs fragments do bind specifically to basophils obtained from allergic and nonallergic children. These antibodies may thus also be employed as tools for studying the human basophils function.

Animals↗
PubMed1994

Fibroblasts determine the fate of Fc epsilon RI+ cell populations in vitro by selectively supporting the viability of mast cells while internalizing and degrading basophils.

To determine the fate of Fc epsilon RI+ cells on fibroblasts in vitro, human bone marrow derived CD34+ cells were cultured in the presence of recombinant human interleukin 3 and recombinant human hematopoietic stem cell factor for 3 weeks, and Fc epsilon RI+ cells were purified by immunomagnetic selection. This enriched Fc epsilon RI+ cell population consisted of 92-94% basophils and 3-5% mast cells as determined by morphologic, immunohistochemical, and ultrastructural criteria. The Fc epsilon RI+ cells were then cocultured with 3T3 fibroblasts. Basophils decreased markedly by 1 week and were absent from cocultures by 2-3 weeks, while the mast cell numbers on the fibroblast monolayers remained constant. Ultrastructural examination of cocultures at 2 days demonstrated phagocytosis of basophils by fibroblasts. By 1 week, phagocytosed basophil membranes and granules gave fibroblasts the superficial appearance of mast cells by toluidine blue staining. Mast cells surviving in cocultures could be distinguished from granule-containing fibroblasts by IgE surface labeling and by ultrastructural demonstration of tryptase-positive granules. Thus, while mast cells remain viable in coculture with 3T3 fibroblasts, basophils do not survive and are internalized and degraded by the fibroblast monolayer.

Basophils↗
PubMedDate not supplied

The interaction of cytokines with human basophils and mast cells.

Human mast cells and basophils participate in allergic inflammation by releasing preformed and newly synthesized mediators upon cross-linking of cell surface IgE/receptor complexes with specific antigen. It is becoming increasingly apparent, however, that the basophil response is up-regulated by a far greater number of cytokines than is the mast cell, making the basophil more sensitive to products that are commonly generated during immune reactions. As a result, basophils may have a greater role in the chronic allergic inflammation that characterizes diseases such as asthma. This belief is supported further by the fact that the basophil has recently been shown to generate interleukin-4, and possibly other cytokines, indicating a role for this cell in directing the immune response of other cell participating in allergic lesions.

Animals↗
PubMedDate not supplied

Regulation of integrin-dependent release in human lung mast cells and basophils.

The interaction of cells with surfaces or components of the extracellular matrix alters cell responses and is regulated by integrins on the cell surface. We have used monoclonal antibodies to CD29 and CD49d followed by an F(ab)2 fragment of rabbit anti-mouse IgG1 to cross-link the integrins on the surface of human lung mast cells and basophils. We found that cross-linking either CD29 or CD49d failed to initiate mediator release from the basophils of non-atopic and atopic donors [histamine release (HR) = 1 +/- 0.5% for CD29 and 1 +/- 0.5% for CD49d, n = 10, NS]. In contrast we found that clustering CD29 caused significant HR from the basophils of asthmatic donors (HR = 21 +/- 5%, n = 10, p < 0.005). Clustering of CD49d also caused significant degranulation in the same donors (HR = 9 +/- 3%, n = 10, p < 0.11). Incubating the basophils of these asthmatic donors with a synthetic RGD peptide significantly reduced CD29- and CD49d-induced histamine release. CS-1 peptide was also found to inhibit CD29-induced histamine release but had no significant effect on CD49d-induced histamine release. The tyrosine kinase inhibitors, genistein and piceatannol, completely ablated CD29- and CD49d-induced degranulation. In summary, we have shown that cross-linking integrins can initiate mediator release from the basophils of asthmatic patients and that this appears to involve recognition of RGD and activation of tyrosine kinase.

Antibodies, Monoclonal↗
PubMed1996

Role of mast cells, basophils and their mediators in adverse reactions to general anesthetics and radiocontrast media.

General anesthetics and radiocontrast media (RCM) can cause anaphylactic or anaphylactoid reactions. These are usually underdiagnosed and underreported, but their incidence is apparently rising. Their pathogenesis is complex and not completely understood, but the release of vasoactive mediators from basophils and mast cells plays a central role. The recent development of in vitro techniques to study the release of preformed (histamine and tryptase) and de novo synthesized mediators (PGD2, LTC4, and PAF) from purified basophils and mast cells has made it possible to quantify the mediator-releasing activity of anesthetics such as muscle relaxants, general anesthetics, opioids, and benzodiazepines and RCM on human basophils and mast cells isolated from lung, skin and heart tissues. The majority of general anesthetics and RCM tested induced only the release of preformed mediators (histamine and tryptase), not of the de novo synthesized eicosanoids. There was wide variability in the response of basophils and mast cells from different donors to the same drug or RCM, presumably due to the releasability parameter. Hyperosmolality is probably not the only factor responsible for basophil and mast cell activation by RCM. The in vitro release of histamine induced by anesthetic drugs and RCM was correlated with the release of tryptase. Given the longer half-life of tryptase than histamine in plasma, measurements of plasma tryptase may become a useful diagnostic tool for identifying adverse reactions to anesthetics and RCM.

Anesthetics, General↗
PubMed1996

Peripheral blood T lymphocytes and basophils, freshly isolated from house-dust-mite-sensitive patients, produce interleukin-4 in response to allergen-specific stimulation.

We examined the capacity of interleukin-4 (IL) production from lymphocytes and basophils, isolated from the peripheral blood of allergic patients sensitive to house dust mite, after stimulation with mite extract. IL-4 production was measured by a sensitive bioassay based on coculture with CT.h4S (a human IL-4-responsive cell line). Lymphocytes and basophils from patients with elevated serum IgE specific to mite allergen [radioallergosorbent test (RAST) score > 3] could produce detectable levels of IL-4 in response to mite extract, whereas those from patients with a RAST score of less than 2 or normal volunteers could not. The sensitivity of basophils to mite extract was high, so that a lower concentration of mite extract (1-10 ng/ml) could induce maximal IL-4 production. On the other hand, a higher concentration (10 micrograms/ml) was required for maximal IL-4 production from the lymphocytes. These findings demonstrate that allergen-specific IL-4-producing cells, lymphocytes and basophils, are generated in vivo in allergic patients and also that there exist characteristic differences between lymphocytes and basophils related to the in vivo source of IL-4.

Allergens↗