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PubMed1993

Basophil histamine release induced by anti-IgE and concanavalin A. Relation to the total plasma IgE content.

The plant lectin concanavalin A (Con A) has been shown to induce basophil histamine release by an IgE-receptor-dependent process resembling that of anti-IgE-antibodies. In this study, the concentration-response for basophil histamine release from washed blood cells was analyzed in a population of blood samples from adults with a total plasma IgE content ranging from < 5 kU/l to > 18,000 kU/l (n = 108), as well as 148 cord blood samples. The concentration-response-curves for anti-IgE in all adult blood samples were similar, despite the large variation in total plasma IgE--only the cord blood samples showed a decreased sensitivity. In contrast, the optimal concentration of Con A was inversely related to plasma IgE, and this relation was most pronounced in the adult blood samples. It is proposed that IgE-receptor-mediated histamine release may be dependent not only on the number of stimulatory, dimeric cross-links formed between IgE-receptors, but also on the molecular structure of the cross-linking agent.

Adult↗
PubMed1994

Mechanisms of eosinophil and basophil migration.

Considerable progress has been made in our understanding of the molecular mechanisms involved in eosinophil and basophil migration into sites of allergic inflammation. It is clearly a staged process, each stage offering a level of control over the cell specificity and degree of migration. On the basis of current evidence, the various receptors and mediators involved are summarized in Table 4. Once in the tissues, eosinophils may persist for several days or weeks, surviving under the influence of locally generated cytokines, and this persistence may also partly explain the selective tissue accumulation of eosinophils and basophils. Understanding the molecular mechanisms involved in leukocyte migration may lead to the discovery of selective and effective antagonists to treat allergic disease by preventing cell migration. Results in a number of animal models already suggest that this approach may be successful. The development of drugs that can be tested in the clinic is awaited with much interest.

Animals↗
PubMed1994

Immune responses to nematode exoantigens: sensitizing antibodies and basophil histamine release.

High levels of IgE and eosinophilia are found in both allergy and helminth infections, but allergic symptoms are rare in naturally acquired helminth infections. The interrelation of specific IgE antibodies and in vitro basophil histamine release (HR) induced by exoantigens from the larval stages (L2/L3) of the nematodes Toxocara canis and Ascaris suum was examined in 148 patients visiting an outpatient clinic for parasitic diseases. The antigen sensitivity of the basophils was found to be dependent not only on the absolute amount of antigen-specific IgE present in patient plasma, but also on the ratio between specific and total IgE. Thus, large HR was observed in some patients in response to helminth antigens despite low levels of both specific and total IgE content in plasma. Patients with eosinophilia showed greater IgE-mediated HR than the other patients examined. In contrast, only five patients showed HR after challenge with anti-IgG4, despite the presence of high levels of antigen-specific IgG4 and IgG1 in all patients showing specific IgE antibodies.

Animals↗
PubMed2006

IgE-receptor activation induces survival and Bfl-1 expression in human mast cells but not basophils.

BACKGROUND: The contribution of mast cells to the pathology of allergic diseases are facilitated by their long life span in tissue and ability to regranulate. Bcl-2 genes are one of the main regulators of cell death and survival. The aim of this study was to elucidate the mechanisms responsible for mast cell survival in allergy. METHODS: Bcl-2 family gene expression in human mast cells and basophils was analyzed by ribonuclease protection assay and by reverse-transcriptase polymerase chain reaction. Cell survival was measured by mixing cells with the vital dye, trypan blue, and the number of living cells was enumerated. Apoptotic cells were measured by a Cell Death Detection ELISA. RESULTS: We found that cross-linking of FcepsilonRI on human cord blood cultured mast cells (CBCMCs) promoted cell survival and induced expression of the pro-survival gene Bfl-1. CBCMCs were found to express both Bfl-1 and Bfl-1S, two splicing variants of Bfl-1. Bfl-1 induction was mediated through Syk, PI3-kinase and intracellular calcium mobilization, since piceatannol, wortmannin and EDTA, respectively, significantly reduced Bfl-1 expression levels. In contrast to CBCMCs, no evidence was found for Bfl-1 expression and survival promotion in human basophils. CONCLUSIONS: Immunoglobulin E (IgE)-dependent activation-induced mast cell survival was correlated with Bfl-1 gene upregulation, providing a possible explanation for mast cell longevity in allergic reactions.

Basophils↗
PubMed2006

Detection of novel leukocyte differentiation antigens on basophils and mast cells by HLDA8 antibodies.

BACKGROUND: Basophils (BA) and mast cells (MC) are important effector cells in allergic reactions. Development, growth and effector cell functions are regulated by a network of cytokines, other ligands, and respective cell surface antigens. METHODS: We examined the expression of novel CD antigens on human BA, lung MC, the BA cell line KU-812, and the MC line HMC-1. Expression of surface antigens was analyzed by monoclonal antibodies (mAb) of the HLDA8 workshop and flow cytometry. RESULTS: Basophils were found to stain positive for CXCR1 (CD181), CCR1 (CD191), CCR2 (CD192), CCR7 (CD197), IL-18Ralpha (CDw218a), IL-18Rbeta (CDw218b), TRAIL-R1 (CD261), TRAIL-R2 (CD262), TACI (CD267), TLR-4 (CD284), LAIR1 (CD305), EMR-2 (CD312), JAM1 (CD321), and JAM2 (CD322). Lung MC were found to react with mAb against EMR-2 (CD312) and JAM1 (CD321). KU-812 cells were found to stain positive for CXCR1 (CD181), TRAIL-R2 (CD262), B7H2 (CD275), TLR-4 (CD284), JAM1 (CD321), and E-Cadherin (CD324). HMC-1 cells were recognized by mAb against TRAIL-R2 (CD262), B7H2 (CD275), LAIR1 (CD305), EMR-2 (CD312), JAM1 (CD321), and Siglec-6 (CDw327). CONCLUSIONS: Extensive phenotyping with antibodies against novel CD antigens provides further evidence that BA and MC represent two separate hematopoietic cell lineages with unique phenotypic properties observed in mature cells as well as malignant immature cells. Further studies are required to define the functional role of these CD antigens expressed in BA and MC.

Antibodies, Monoclonal↗
PubMed2006

Basophil Activation Test and specific IgE measurements using a panel of recombinant natural rubber latex allergens to determine the latex allergen sensitization profile in children.

There are no documented studies that describe natural rubber latex (NRL) sensitization in children with a history of surgical intervention but without any congenital malformation (urogenital anomalies, spina bifida, etc.), although some authors have studied NRL allergy in children without a history of surgical intervention. The aim of this work was to evaluate the sensitization profile to single NRL allergens in children without spina bifida and without repeated surgical interventions, by using different recombinant and natural latex allergens in two analytical techniques: specific serum immunoglobulin E (IgE) quantification and flow cytometry determination of activated basophils expressing CD63, after stimulating cells from patients with NRL allergens. A total of 23 patients and 10 healthy children were selected. Conjunctival and in-use NRL provocation tests were carried out, as well as specific IgE determination in all patients' and controls' sera with the recombinant NRL allergens: rHev b 1, rHev b 2, rHev b 3, rHev b 5, rHev b 6.01, rHev b 6.02, rHev b 8, rHev b 9 and rHev b 11 and with NRL (k82) using appropriate ImmunoCAPs. The Basophil Activation Test (BAT) was performed with whole latex extract and with the recombinant allergens rHev b 5 and rHev b 6.01, as well as with the natural allergen Hev b 6.02. The sensitivity and the specificity of NRL-specific IgE (k82) were 100%. Positive IgE responses to rHev b 5 were found in sera of 10 children, to rHev b 6.01 in 16 and for rHev b 6.02 in 15 children's sera. Specific IgE to rHev b 8 was found in four sera of the children. We only found significant differences in sensitization to rHev b 5 in children with two or more surgical interventions compared with the non-intervened group or those with only one intervention. Specific IgE in sera of children with latex-fruit syndrome recognized rHev b 6.02, but not to rHev b 11. The patients sensitized to Hev b 8, Hev b 9 and/or Hev b 11 were atopic. The four patients presenting a positive response to the NRL profilin Hev b 8 were allergic to pollen. The BAT against whole NRL extract was positive in 22 of 23 children; against rHev b 5 in 14 of the patients studied; against rHev b 6.01 in seven cases and against nHev b 6.02 in 19 children. In all the control subjects, the results using this technique were negative. If combined rHev b 5, rHev b 6.01 and nHev b 6.02 together, BAT could detect 20 of the 23 children with latex allergy. The combined use of ImmunoCAP with all the recombinant NRL allergens and BAT with rHev b 5, rHev b 6.01 and nHev b 6.02, enabled the identification of NRL allergy in 22 of 23 patients. There is a positive and significant correlation between sensitization to Hev b 5 and the number of interventions. BAT and allergen-specific IgE determination could be used as first-line in vitro diagnostic tests in patients with NRL allergy.

Adolescent↗
PubMed1996

Effect of lidocaine on histamine release and Ca2+ mobilization from mast cells and basophils.

BACKGROUND: Various anesthetic drugs have been known to induce allergic reactions, which have been caused by histamine release from mast cells/basophils. Although lidocaine is reported to suppress allergic reactions, there have been no reports about lidocaine's direct effects to inhibit histamine release from mast cells/basophils. METHODS: We examined the effect of lidocaine on histamine release in vitro from freshly extracted as well as cultured mast cells and basophils. Additionally, the effects of lidocaine on intracellular calcium concentration were monitored by assessing Fura-2 signals in cultured cells. RESULTS: Lidocaine (10(-3)-10(-2) M: approximately 234-2340 micrograms/ ml) inhibited both the IgE-dependent and IgE-independent histamine release from all mast cells/basophils in a dose-dependent manner. However, lidocaine inhibited the IgE-dependent response more than the IgE-independent response (P < 0.01). Lidocaine also inhibited increases in intracellular Ca2+ to a greater extent after IgE-dependent stimulation as compared with IgE-independent stimulation. The degree of the inhibition of histamine release by lidocaine appeared to parallel decreases in Ca2+ mobilization. CONCLUSIONS: Our results indicate that lidocaine directly inhibits histamine release from both rodent mast cells and human basophils in vitro at concentrations from 10(-3) to 10(-2) M (234 to 2340 micrograms/ml). That may be influenced by Ca2+ mobilization. Although these results are not immediately relevant to clinical practice, allergic reaction caused by direct effect of lidocaine seems to be impossible.

Anesthetics, Local↗
PubMed1991

Inhibition by galanin and by high K+ of human basophil histamine release triggered by calcium ionophores but not responses induced by anti-IgE, chemotactic peptide or phorbol ester.

1. Galanin concentration-dependently blocked human leukocyte histamine release triggered by the calcium ionophores A23187 and ionomycin. Almost complete inhibition of release was recorded at 410 nM whereas 41 nM galanin mediated close to 50% inhibition of responses. 2. Pretreatment of the cells with pertussis toxin did not influence the inhibitory effects of galanin. 3. Leukocyte responses triggered by anti-IgE, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) or 4 beta-phorbol 12-myristate 13-acetate (PMA) were not affected by galanin. 4. Ionophore-induced basophil histamine release, but not responses triggered by anti-IgE, FMLP or PMA, was inhibited when cells were challenged in medium containing high potassium (120mM). 5. We conclude that galanin and a depolarizing medium selectively inhibit ionophore-induced basophil histamine release.

Basophils↗
PubMed1989

Basophil histamine release and leukotriene (LTB4-LTC4) production in cluster headache.

Histamine release and leukotrienes (LTB4 and LTC4) production from circulating basophil have been studied in 13 patients with episodic cluster headache (CH) during the remission phase of symptoms, and in 9 normal subjects. Cell suspensions of basophils were stimulated with scalar dilutions of anti-IgE, f-met-peptide and Ca2+ ionophore A23187. Histamine was measured by an automated fluorimetric method; LTB4 and LTC4 with RIA in individual cases, and with Reverse-Phase HPLC in the two pools obtained from the supernatants of CH patients and controls. Mean values of histamine release in patients with CH were significantly lower when compared to those obtained in control subjects after stimulation with anti-IgE at the three dilutions used. LTC4 mean levels measured in CH patients were significantly lower than those of supernatants from controls after stimulation with 0.05 gamma/ml of A23187. A reduction of LTC4 and LTB4 levels in CH patients was also observed in R-P HPLC, which showed different elution patterns in the two groups. The histamine release in individual cases was related to leukotriene production: LTC4 levels were significantly (p less than .05) higher in "high histamine releasers" than in "low histamine releasers". Our results indicate that CH patients have complex abnormalities of histamine release and of leukotriene production during the painless phase of the disease.

Adult↗
PubMed1988

Induction of human basophil histamine release by a novel protein kinase C activator, sn-1,2-isopropylidene-3-decanoyl-glycerol (IpOCOC9): partial characterization of secretagogue characteristics.

Human leukocytes were found to release histamine at exposure for the synthetic glyceride derivative sn-1,2-isopropylidene-3-decanoyl-glycerol (IpOCOC9). The following characteristics for the IpOCOC9-induced basophil histamine release were recorded. A. In the order of 25% of the cellular histamine content was extruded at 206 mumol/l and 45% at 690 mumol/l of the compound, respectively. B. Removal of extracellular Ca2+ variably affected IpOCOC9-triggered release. C. The presence of N-ethylmaleimide (10 mumol/l) or p-bromophenacylbromide (10 mumol/l) markedly reduced IpOCOC9-induced histamine release. D. The time course of the release triggered by IpOCOC9 was intermediate to those characterizing the release triggered by 4 beta-phorbol 12-myristate 13-acetate (PMA) and by formyl-methionyl-leucyl-phenylalanine (FMLP). E. Cells desensitized to IgE-receptor-mediated stimulation were hyperresponsive to stimulation with IpOCOC9. F. Cells treated with a low concentration of 2-deoxyglucose were not hyperresponsive to IpOCOC9. These data show that IpOCOC9, a PMN/leukocyte protein kinase C stimulator, acts as a non-cytotoxic secretagogue for human basophils with a mode of action which in some, but not all respects, mimics that of PMA. In particular, IpOCOC9-triggered release resembles that reported by other authors for hyperosmolar triggering of release by mannitol.

Acetophenones↗
PubMed1984

Allergic and pseudo-allergic reactions caused by penicillins, cocoa and peppermint additives in penicillin factory workers examined by basophil histamine release.

Allergic and pseudo-allergic reactions were examined in penicillin factory workers exposed to the dust of preparations of pivampicillin and pivmecillinam. Among 14 workers basophils from five persons showed histamine release by challenge with penicillins, whereas no release was observed in controls of non-atopic individuals not working with the manufacturing of penicillin. Positive skin response was obtained in four workers by path testing and in three persons by scratch test revealing late but no immediate response. All the eight workers who were also exposed to flavour additives used in the penicillin preparations showed histamine release by cocoa and peppermint. The release was not changed by removal of immunoglobulins from the basophil cell surface and the additives caused a similar release in the controls. The histamine release caused by cocoa and peppermint therefore depend on non-immunological mechanisms, i.e. pseudo-allergic reactions which might contribute to the symptoms in penicillin factory workers.

Allergens↗
PubMed1988

Characterisation of IgE-mediated histamine release from equine basophils in vitro.

In vitro IgE-mediated histamine release by equine blood basophils was characterised as the basis for a screening test for immediate hypersensitivity responses in horses. The responses are initiated by inducing agents that are capable of crosslinking or bridging the membrane-bound IgE molecules. The release process is complete within 40 mins. In vitro histamine release is dose-dependent, with a submaximal response at less or greater than the optimal dose of inducing agent. Exogenous calcium is required but not magnesium; the optimal release calcium concentration is 1.0 to 1.5 mM. If an IgE-mediated inducing agent is added in the absence of exogenous calcium, the basophils become desensitised. The pH and temperature optima for release are physiological (pH 7.4, 37 degrees C). Histamine release is potentiated by deuterium oxide.

Animals↗
PubMed2006

Agonist and antagonist effects of 15R-prostaglandin (PG) D2 and 11-methylene-PGD2 on human eosinophils and basophils.

Prostaglandin (PG) D2 acts through both the DP(1) receptor, which is coupled to adenylyl cyclase, and the DP2 receptor (chemoattractant receptor-homologous molecule expressed on Th2 cells), which is present on eosinophils, basophils, and Th2 cells and results in cell activation and migration. The most potent prostanoid DP2 agonist so far reported is 15R-methyl-PGD2, in which the hydroxyl group has the unnatural R configuration. In contrast, the corresponding analog possessing the natural 15S configuration is approximately 75 times less potent. This raised the question of whether the isoprostane 15R-PGD2 might have potent DP2 receptor-mediated biological activity. We therefore chemically synthesized 15R-PGD2 and investigated its biological activity. This compound elicited DP2 receptor-mediated CD11b expression in human basophils and eosinophils and induced actin polymerization and migration in eosinophils with a potency about the same as that of PGD2. In contrast, it had only a weak effect on DP1 receptor-mediated adenylyl cyclase activity in human platelets. We also investigated the effects of modification of the 9-hydroxyl and 11-oxo groups of PGD2. Both PGK2, in which the 9-hydroxyl group is replaced by an oxo group, and 11-deoxy-11-methylene PGD2, in which the 11-oxo group is replaced by a CH2 group, have little or no DP1 or DP2 agonist activity. However, the 11-methylene analog is a DP2 antagonist (IC50, approximately 2 microM). We conclude that 15R-PGD2, which may be generated by oxidative stress, is a potent and selective DP2 agonist and that modification of the 11-oxo group of PGD2 can result in DP2 antagonist activity.

Actins↗
PubMed1988

Induction of histamine release from rat mast cells and human basophilic granulocytes by clinical Escherichia coli isolates and relation to hemolysin production and adhesin expression.

We investigated the role of 27 disease-relevant Escherichia coli strains isolated from humans in the induction of histamine release from rat peritoneal mast cells and human basophilic granulocytes. Our data indicated that only the hemolysin-positive (HLY+) bacteria and the hemolysin-positive culture supernatants induced histamine release. For the latter, the hemolysin activity determined the degree of histamine secretion. Incubation of the target cells with washed HLY+ bacteria revealed a different secretory response. For the rat mast cells, histamine release paralleled expression of hemolysin activity, with the exception of strain S98 (O75:K5:H- HLY+), which induced less histamine, although its hemolysin activity was relatively high. No correlation between histamine secretion and hemolysin activity was observed when human basophils were stimulated with the HLY+ bacteria. Large amounts of histamine were still released, even when the hemolysin activity declined to zero. Our results support the potent role of the E. coli hemolysin as a pathogenicity factor in bacterial infection.

Adhesins, Escherichia coli↗
PubMed1999

Role of protein phosphatases in the regulation of human mast cell and basophil function.

Many extracellular stimuli mediate physiological change in target cells by altering the phosphorylation state of proteins. These alterations result from the dynamic interplay of protein kinases, which mediate phosphorylations, and protein phosphatases, which catalyse dephosphorylations. The antigen-mediated aggregation of high-affinity receptors for IgE on mast cells and basophils triggers rapid changes in the phosphorylation of many proteins and culminates in the generation of inflammatory mediators involved in allergic inflammatory diseases such as asthma. Although protein kinases have an established role in this process, less is known about the involvement of protein phosphatases. This imbalance has been redressed in recent years by the availability of phosphatase inhibitors, such as okadaic acid, that facilitate investigations of the role of protein phosphatases in intact cells. Here we review a number of studies in which inhibitors of protein phosphatases have been used to shed light on the potential importance of these enzymes in the regulation of human mast cell and human basophil function.

Basophils↗
PubMedDate not supplied

Mechanisms and pharmacologic control of basophil-derived IL-4 and IL-13.

Human basophils represent a major source of interleukin (IL) 4 and 13 protein, cytokines which share several biological activities central to the pathogenesis of allergic inflammation. Studies show that the production of these cytokines differs with respect to mode of activation and the time course of their secretion. Pharmacologic evidence indicates that IL-4 generation, which is most prominent with IgE-dependent activation, is mediated through a calcineurin-dependent pathway. In contrast, multiple pathways seem evident in the regulation of IL-13 in basophils.

Autocrine Communication↗
PubMed2002

Nonreceptor protein tyrosine and lipid phosphatases in type I fc(epsilon) receptor-mediated activation of mast cells and basophils.

Protein tyrosine and lipid phosphorylations are early and critical events in type 1 Fc(epsilon) receptor (Fc(epsilon)RI)-mediated activation of mast cells and basophils. Tyrosine phosphorylation of Fc(epsilon)RI subunits as well as other signal transduction molecules reflects the balance between the action of protein tyrosine kinases and phosphatases. Similarly, the phosphate content of inositol phospholipids, involved in the recruitment of signalling molecules to the plasma membrane and the generation of secondary messengers, is the net result of the opposing effects of phosphoinositide kinases and lipid phosphatases. This review summarizes the current understanding of the structural and functional aspects of nonreceptor protein tyrosine phosphatases (SHP-1, SHP-2, HePTP, PTP20, PRL1, PRL2, PTP-MEG1 and PTP-MEG2) and lipid phosphatases (SHIP and SHIP2) in the activation of mast cells and basophils after Fc(epsilon)RI aggregation. New approaches towards a deeper understanding of the role of phosphatases in mast cell physiology are also discussed.

Basophils↗
PubMed2005

A comparative study of the FcepsilonRI molecule on human mast cell and basophil cell lines.

BACKGROUND: Mast cells and basophils express the high-affinity IgE receptor FcepsilonRI. We have analysed the human mast cell line LAD2 and four subclones of the basophil cell line KU812 in order to reveal possible differences concerning the FcepsilonRI surface regulation, anti-IgE-triggered activation, FcepsilonRIalpha protein stability and the mRNA level of FcepsilonRIalpha-, beta- and the truncated beta-chain (beta(T)), and thereby determine the utility of these cell lines in investigations of the FcepsilonRI biology. METHODS: The surface expression of FcepsilonRI was assessed by flow cytometry, using the monoclonal antibody CRA1. The FcepsilonRI-induced cellular activation (i.e. cross-linking of FcepsilonRI) was determined by changes in the intracellular level of Ca2+, which was measured by fluorescence of Fura-2. The level of the FcepsilonRIalpha protein was determined by a Western blot technique and by a radioimmunoassay. The mRNA level of FcepsilonRIalpha, beta- and beta(T)-chain was analysed using real-time PCR. RESULTS: Two KU812 subclones and especially LAD2 had FcepsilonRI surface expression which was capable of inducing cellular activation. Both the FcepsilonRI expression and stability of the FcepsilonRIalpha protein were increased when IgE was present. All the cell lines expressed mRNA of FcepsilonRIalpha-, beta- and beta(T), with LAD2 tending to have the highest expression. However, a determination of the beta/beta(T) ratio demonstrated no difference between any of the cell clones. CONCLUSION: These cell lines are important tools in the investigation of both the FcepsilonRI molecule and the effects induced by its activation.

Basophils↗