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PubMed2006

Inhibition of rBet v 1-induced basophil histamine release with specific immunotherapy -induced serum immunoglobulin G: no evidence that FcgammaRIIB signalling is important.

BACKGROUND: Human basophils and mast cells express the low-affinity immunoglobulin (Ig)G receptor FcgammaRIIB. It has previously been shown in artificial model systems that cross-linking of the high-affinity IgE receptor FcepsilonRI and FcgammaRIIB leads to inhibition of FcepsilonRI signalling. OBJECTIVE: The aim of the present study was to investigate whether cross-linking of FcepsilonRI and FcgammaRIIB contributes to IgG-mediated inhibition of histamine release in human basophils in a system using the sera from specific immunotherapy (SIT) patients and the major allergen from birch pollen, Bet v 1. As IgG4 furthermore has been proposed to have special blocking properties, we investigated the significance of IgG subclass specificity for this inhibition. METHODS: Binding of recombinant Bet v 1-IgG complexes to FcgammaRII and IgG-binding activities in the sera from 25 birch pollen-allergic patients treated with SIT were measured using (125)I-rBet v 1. Inhibition of basophil histamine release was assessed by incubating washed leucocytes with complexes of rBet v 1-IgG with or without blocking of FcgammaRII. RESULTS: We observed low binding of rBet v 1-IgG complexes to FcgammaRII, which was negatively correlated with the relative IgG4-binding activities. Blocking of FcgammaRII did not reverse the SIT-IgG-induced inhibition of basophil histamine release. However, IgG-binding activities correlated significantly with the ability of the SIT sera to inhibit basophil histamine release. CONCLUSION: We suggest that at least in birch pollen SIT, the contribution of FcgammaRIIB-mediated inhibitory signalling to SIT-IgG-induced inhibition of human basophil histamine release is of minor importance. The main contributor to the inhibitory effect of SIT-induced IgG seems to be blocking of the allergen-IgE interaction.

Allergens↗
PubMed2006

Evidence of in vivo basophil activation in chronic idiopathic urticaria.

BACKGROUND: Approximately 40% of chronic idiopathic urticaria (CIU) subjects have autoantibodies to either FcepsilonRIalpha or IgE. The effect of such autoantibodies on circulating basophil activation status is unknown. OBJECTIVE: The expression of cell surface activation markers on basophils from CIU, non-allergic, and allergic subjects were compared. Further, the relationship between marker expression and serum factors reported in CIU, such as histamine-releasing activity (HRA) and immunoreactivity to FcepsilonRIalpha were examined. METHODS: Peripheral blood was obtained from CIU, allergic, and non-allergic donors and fractionated by density gradients. Enriched basophils (1-12%) were analysed by flow cytometry for expression of activation markers including CD63, CD69, and CD203c. Dilutions of serum (5-50%) were analysed for HRA on basophils from a normal donor. Serum was tested for immunoreactivity by western blotting to a standard cell lysate prepared from an RBL-SX38 cell line transfected with human FcepsilonRIalpha. RESULTS: CIU subjects (n=9) and allergic subjects (n=8) exhibited enhanced expression of CD63 and CD69, as compared with non-allergic subjects (n=7); however, no difference was seen among groups for CD203c expression. Five CIU and two non-allergic subjects had evidence of significant serum HRA (>20%), whereas two CIU, two allergic, and three non-allergic subjects had evidence of serum immunoreactivity to FcepsilonRIalpha. Serum HRA and serum immunoreactivity to FcepsilonRIalpha were not associated with enhanced surface marker expression. CONCLUSION: Basophil activation marker expression is increased in CIU subjects and is not associated with serum factors. In addition, serum HRA and FcepsilonRIalpha immunoreactivity are not unique to CIU, or related to enhanced circulating basophil marker expression.

Antigens, CD↗
PubMed1996

Basophil counts on the technicon H*1 automated counter.

The precision, accuracy, stability and clinical usefulness of the basophil count of a Technicon H*1 automated blood cell counter were assessed and a reference range for the absolute basophil count was derived. As expected, the precision was considerably better than that of a manual count but it was worse than would have been expected if the only inaccuracy were the random error consequent on the number of cells counted. Accuracy was sufficient for the count to be of some clinical use but an elevated 'basophil' count was more often consequent on 'pseudo-basophilia' than on true basophilia. As a consequence it is necessary to confirm elevated counts by microscopic examination of a blood film whenever the presence of an elevated count is diagnostically important. The basophil count was stable for up to 3 days, both at room temperature and at 4 degrees C. The reference range was 0.02-0.09 x 10(9)/I. An elevated 'basophil' count serves to alert the instrument operator to the presence of an abnormal blood sample. Since the technology used to count basophils is the same in H*1, H*2 and H*3 instruments, our results can be generalized to other instruments in the series.

Basophils↗
PubMed1994

The surface membrane antigen phenotype of human blood basophils.

Basophils are effector cells of allergic reactions and express a unique profile of cellular antigens (Ag). Using a combined toluidine-blue/immunofluorescence staining method, we were able to study the cell membrane Ag phenotype of normal human blood basophils with monoclonal antibodies (mAbs) against established and novel CD antigens. According to previous findings, basophils express CD9 (p24), CD11a (LFA-1 alpha-chain), CD11b (C3biR), CD11c (CR4), CD13 (aminopeptidase N), CDw17 (lactosylceramide), CD18 (beta-chain of beta 2), CD25 (IL-2R alpha-chain), CD26 (dipeptidylpeptidase), CD31 (PECAM), CD35 (CR1), CD38 (T10), CD43 (leukosialin), CD44 (Pgp-1), CD45 (pan-leukocyte Ag), and CD63 (basophil activation Ag). Various novel CD Ags were detected on basophils, including membrane cofactor protein (MCP) (CD46), the N-linked glycan CD47, decay-accelerating factor (DAF) (CD55), membrane attack complex inhibitory factor (MACIF) (CD59), LFA-3 (CD58), ICAM-2 (CD 102), ICAM-3 (CD50), C5a receptor (CD88), MIC-2/E2 (CD99), and the interleukin-1 (IL-1) R type II (CD121b). These data provide further evidence that basophils express a unique profile of surface membrane receptors for cytokines and immunomodulating compounds, as well as adhesion molecules and surface glycolipids.

Antigens, Surface↗
PubMed1998

Is tyrosine kinase activation involved in basophil histamine release in asthma due to western red cedar?

Occupational asthma due to western red cedar is associated with histamine release from basophils and mast cells on exposure to plicatic acid (PA), but the mechanisms underlying this response remain unclear. Specific kinase inhibitors were used to study the role of tyrosine and serine/threonine kinases in PA-induced histamine release from human basophils. Pretreatment with the tyrosine kinase inhibitor methyl 2,5-dihydroxy-cinnamate (MDHC) attenuated histamine release from basophils triggered by anti-IgE (29.8% inhibition; n = 15; P < 0.01) or grass pollen (48% inhibition; n = 6; P < 0.01). Inhibition was concentration-dependent and could be reversed by washing the cells in buffer, while the inactive stereoisomer of MDHC did not affect histamine release. In contrast, the protein kinase C inhibitor staurosporine did not affect histamine release by either anti-IgE or grass pollen. Pretreatment with MDHC partially inhibited PA-induced histamine release from basophils of 6/9 patients with red cedar asthma (25.4% vs 33.8%; P = NS). Staurosporine gave a similar level of inhibition of PA-induced histamine release (25.3% vs 33.8%; P = NS). Thus, signal transduction of the human basophil Fc epsilon RI appears to depend upon tyrosine kinase activation, but not on protein kinase C (serine/threonine kinase) activation. The lack of specific effect on plicatic acid-induced histamine release in basophils obtained from patients with occupational asthma due to western red cedar suggests that tyrosine kinases are not as important in this disease as in atopic asthma, and is consistent with the view that histamine release in red cedar asthma is largely IgE-independent.

Allergens↗
PubMed1995

Cytokines involved in growth and differentiation of human basophils and mast cells.

Mast cells and basophils are multifunctional effector cells of the immune system. Both are myeloid cells and originate from multipotent hemopoietic progenitor cells. Usually, human basophils complete their differentiation in the bone marrow. In contrast, mast cells usually undergo differentiation in extramedullary organs. During the past few years, growth factors for human basophils and a growth factor for human mast cells have been identified. Interleukin-3 is the most potent differentiation factor for human basophils and activates mature basophils via high affinity binding sites. Other basophil agonists are GM-CSF, IL-5, NGF and certain chemokines (IL-8, MCP-1). Mast cells apparently loose cytokine binding sites during mastopoiesis and as mature cells, do not express detectable amounts of IL-3R, GM-CSFR or IL-8R. However, in contrast to other myeloid cells, mast cells express SCF receptor/c-kit during mastopoiesis and on mature cells. Furthermore, the ligand of c-kit, SCF, induces differentiation of human mast cells from their progenitor cells and upregulates effector functions in mature mast cells.

Animals↗
PubMed1987

Mechanism of activation of human basophils by Staphylococcus aureus Cowan 1.

We investigated the capacity of Staphylococcus aureus Cowan 1 and S. aureus Wood 46 to induce histamine release from human basophils in vitro. S. aureus Cowan 1 (10(5) to 10(7)/ml), which synthesizes protein A (Staph A), stimulated the release of histamine from basophils, whereas S. aureus Wood 46 (10(5) to 2 X 10(7)/ml), which does not synthesize Staph A, did not induce histamine secretion. Soluble Staph A (10(-3) to 10 micrograms/ml), but not staphylococcal enterotoxin A, induced histamine secretion from human basophils. Staph A binds through its classical site to the Fc region of human immunoglobulin G (IgG) and through its alternative site to the Fab portion of the different human immunoglobulins. Hyperiodination of Staph A, which destroys over 90% of the original Fc reactivity without altering the Fab-binding site, did not alter the ability of the protein to induce histamine release. The stimulating effect of Staph A was dose dependently inhibited by preincubation with human polyclonal IgG (0.3 to 100 micrograms/ml) and a human monoclonal IgM (0.3 to 100 micrograms/ml) which have F(ab')-Staph A reactivity. In contrast, rabbit IgG, which possesses only Fc-Staph A reactivity, and a Staph A-unreactive human monoclonal IgM did not inhibit Staph A activity. Similar results were obtained with intact S. aureus Cowan 1. Preincubation with either Staph A or anti-IgE (rabbit anti-Fc epsilon) resulted in complete desensitization to a subsequent challenge with the homologous stimulus. Staph A and anti-IgE induced partial cross-densensitization to the heterologous stimulus. Cells preincubated with anti-IgG (rabbit anti-Fc gamma) lost a small but significant part of their ability to release with Staph A but did not lose their response to anti-IgE. Basophils from which IgE had been dissociated by brief exposure to lactic acid no longer released histamine in response to anti-IgE and Staph A. When basophils from which IgE had been dissociated were incubated with human polyclonal IgE, they regained their ability to induce histamine in response to Staph A and anti-IgE. In contrast, two monoclonal IgEs which do not bind to Staph A did not restore the basophil responsiveness to Staph A. Furthermore, there was complete cross-desensitization between soluble Staph A and S. aureus Cowan 1, while cells desensitized to S. aureus Wood 46 released normally with Staph A and S. aureus Cowan 1.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1998

Exogenous nitric oxide regulates the degranulation of human basophils and rat peritoneal mast cells.

This study was designed to investigate whether anti-IgE-induced or ionophore A23187-induced histamine release from human basophils is regulated by exogenous nitric oxide (NO), and to assess some similarities between the effect of NO on basophils and that on rat peritoneal mast cells (RPMC). The NO donor, sodium nitroprusside (SNP), inhibited A23187-induced histamine release from crude human basophils and crude RPMC in a dose-dependent fashion. This downregulation was still observed when SNP was washed out just before the cell stimulation, indicating that the effect of SNP was irreversible. The downregulation disappeared in both purified cell populations after the removal of contaminating cells. However, when purified cells were preincubated with SNP in the presence of 5 mM N-acetylcysteine (NAC), increasing the bioavailability of NO, the downregulation was recovered. The presence of NAC significantly augmented the downregulation of SNP on A23187-induced histamine release from both crude cell populations. In contrast, SNP had no effect on anti-IgE-induced histamine release from either crude or purified basophil preparation in the absence of NAC, and SNP plus NAC inhibited anti-IgE-induced histamine release from both cell preparations. The same results were obtained with crude and purified RPMC preparations under the same conditions. These results show that SNP similarly downregulated exocytosis of basophils and RPMC, and acquired the potent effect in the presence of NAC, indicating that exogenous NO plays a part in the regulation of basophil and mast cell activation.

Acetylcysteine↗
PubMed2001

Hymenoptera-venom-induced upregulation of the basophil activation marker ecto-nucleotide pyrophosphatase/phosphodiesterase 3 in sensitized individuals.

BACKGROUND: Bee and wasp venoms are potent allergens capable of inducing severe clinical reactions. To detect immediate-type hypersensitivity to these allergens, a rapid in vitro test was developed that relies on the upregulation of ecto-nucleotide pyrophosphatase/phosphodiesterase 3 (E-NPP3) on activated basophils. METHODS: Blood basophils of 13 healthy donors and 22 patients allergic to bee or wasp venom were analyzed for E-NPP3 (CD203c) expression using monoclonal antibody 97A6. Basophils were analyzed by flow cytometry after activation with anti-IgE antibody or allergen. Venom-induced E-NPP3 upregulation on basophils was compared with diagnostic parameters, including skin tests and assessment of specific IgE. In selected samples, the increase in E-NPP3 expression on activated basophils was compared with histamine release and CD63 upregulation. RESULTS: In 20/22 patients sensitized to wasp or bee venom, E-NPP3 expression on basophils was upregulated in response to activation by allergen or anti-IgE. The maximum increase in E-NPP3 expression (above ten times of baseline) was achieved after 15 min of stimulation with 1 microg/ml of allergen or anti-IgE antibody. Sensitized individuals who failed to upregulate E-NPP3 in response to IgE receptor cross-linking also failed to induce histamine release and CD63 upregulation. CONCLUSIONS: Flow cytometric determination of hymenoptera-venom-induced upregulation of E-NPP3 is a novel in vitro test to identify sensitized individuals.

Adult↗
PubMed2002

Detection of novel CD antigens on the surface of human mast cells and basophils.

BACKGROUND: Mast cells (MC) and basophils are effector cells of allergic reactions. Growth and function of these cells are regulated by a network of cytokines, other ligands, and respective cell surface membrane receptors. METHODS: In the present study, we examined the expression of novel CD antigens on human lung MC, skin MC, blood basophils, the MC line HMC-1, and the basophil cell line KU-812. Expression of surface antigens was analyzed by monoclonal antibodies (mAbs) and indirect immunofluorescence staining techniques. RESULTS: Primary MC were found to react with mAbs against KIT (CD117), the signal regulatory protein SIRP-alpha (CD172a), and the ectoenzyme E-NPP3 (CD203c). Human basophils were found to express large amounts of E-NPP3 and lower levels of Siglec-5 (CD170), CXCR4 (CD184) and SIRP-alpha. The HMC-1 cell line was recognized by mAbs against SIRP-alpha, CXCR4, endothelial protein C receptor (CD201) and E-NPP3. KU-812 cells were found to react with mAbs against E-NPP3, CXCR4 and glycophorin C (CD236R), but did not react with mAb against endothelial protein C receptor. Most of the other CD antigens tested disclosed negative results. CONCLUSIONS: In summary, our data provide further evidence that MC and basophils express a unique composition of surface antigens. The use of novel CD antibodies may help to isolate MC and basophils and to study their functional properties.

Antibodies, Monoclonal↗
PubMed2005

Differential role for mitogen-activated protein kinases in IgE-dependent signaling in human peripheral blood basophils: in contrast to p38 MAPK, c-Jun N-terminal kinase is poorly expressed and does not appear to control mediator release.

BACKGROUND: Exposure of human basophils to allergens results in a rapid secretion of histamine, LTC(4), IL-4 and IL-13, which dominate both the symptomology of allergic diseases and support the underlying Th2/IgE predominance associated with these reactions. The IgE-dependent release of these mediators in basophils crucially involves PI 3-kinase and the subsequent activation of p38 MAPK and ERK1&2. Here, we investigated the role of the third major member of the mitogen activated kinase family, namely the c-Jun amino terminal kinase (JNK), which is rapidly activated following IgE receptor cross-linking in murine mast cells. METHODS: Human basophils were highly purified by magnetic cell sorting. The activities of various intracellular signaling components, in basophils that had been stimulated under various conditions, were assessed by Western blotting. Mediator secretions were also determined using either spectrofluorometric analysis (histamine) or ELISA (LTC(4), IL-4 and IL-13). RESULTS: Our results show that while JNK is moderately expressed in human basophils, it is not consistently phosphorylated upon anti-IgE stimulation. Phosphorylation of the transcription factor c-Jun, a downstream target of JNK, was also undetected in contrast to p38 MAPK and ERK1&2, which were clearly activated following anti-IgE stimulation of the cells. Additionally, inhibitors of the JNK pathway failed to prevent basophil mediator release and had no effect on the phosphorylation of p38 MAPK or ERK1&2 at concentrations which were specific for JNK blockade. CONCLUSIONS: These data suggest major differences in utilizing various members of the mitogen-activated kinase family in the signal transduction cascade of IgE-receptor-bearing cells.

Basophils↗
PubMed1993

CGP 41251, a novel protein kinase inhibitor with in vitro selectivity for protein kinase C, strongly inhibits immunological activation of human skin mast cells and human basophils.

The process of high-affinity IgE receptor (Fc epsilon RI)-mediated signal transduction in human basophils and mast cells is accompanied by activation of protein kinase C (PKC). The present study investigated the effects of a novel protein kinase inhibitor with in vitro selectivity for PKC (CGP 41251) in comparison with the potent but non-selective PKC inhibitor staurosporine on the activation of human peripheral basophilic leukocytes and enzymatically isolated human skin mast cells. CGP 41251 exerted strong concentration-dependent inhibitory effects on Fc epsilon RI-mediated histamine release from both cell populations. In addition, the IgE-mediated generation of arachidonic acid metabolites (leukotriene C4/D4 and prostaglandin E2) from human basophils was also significantly inhibited by this compound. Its action was not significantly different from the action of staurosporine. Direct activation of cellular PKC by the phorbol ester 12-o-tetradecanoyl-phorbol-13-acetate and subsequent histamine release from basophils was also inhibited by both compounds. CGP 41251 did not suppress N-formyl-met-leu-phe- or A23187-induced activation of basophils, whereas A23187-induced mediator release from human skin mast cells was inhibited in a concentration-dependent fashion. We conclude that an increase of in vitro selectivity for PKC does not significantly enhance inhibitory effects on immunological activation of histamine-containing cells. Moreover, nonimmunological pathways of signal transduction in basophils and mast cells appear to be mediated by distinct biochemical events.

Alkaloids↗
PubMed1986

In vitro appearance of large human histamine-containing basophilic cells.

The appearance of large human basophilic cells containing histamine was followed to reflect cell maturation in cultures of peripheral blood leukocytes. Aliquots were taken on day 0 and after 7, 9-10 and 14 days in culture, and the basophilic cell numbers were determined in 200 microliter cytospin specimens stained with Wright's stain. The number of small basophils initially present declined during the culture period. The number of spontaneously appearing large basophilic cells varied among the cultures from different individuals and was slightly, though not significantly, higher in atopic individuals than in normals. In cultures of cells from atopic individuals, the number of large basophilic cells was reproducibly increased by the addition of appropriate allergen to the cultures. In cultures of cells from normal individuals, the number was increased two- to six-fold by adding conditioned medium (CM), either from 3-day cultures of cells from atopic individuals stimulated with allergen or with CM from the Mo T cell leukemic line. The addition of mitomycin C decreased the number of large basophilic cells and cycloheximide abrogated their appearance.

Allergens↗
PubMed1988

Human basophilic cell differentiation promoted by 2.5S nerve growth factor.

In liquid cultures of human cord blood mononuclear cells, the activities of the 2.5S nerve growth factor (NGF) inducing basophil and eosinophil differentiation were investigated. Various concentrations of immunopurified 2.5S NGF derived from murine submaxillary glands were added to cultures with or without conditioned medium from a human T cell line (Mo-CM), which has previously been shown to produce activities stimulating granulocyte-macrophage colonies. Addition of NGF led to significant increases in differentiation of basophilic cells accompanied by histamine synthesis at 2 weeks in vitro; eosinophil differentiation was not increased in these cultures. In addition, NGF could be shown to amplify basophil differentiation induced by Mo-CM, and the activity of NGF inducing basophil differentiation was dependent on the presence of T lymphocytes. These results indicate that NGF stimulates T-lymphocyte-dependent basophilic cell differentiation from human cord blood progenitors and may in this way support differentiation of basophils or mast cells in vivo at sites of allergic tissue inflammation.

Basophils↗
PubMed1990

Further characterization of surface membrane structures expressed on human basophils and mast cells.

Recently, we were able to establish the immunologic surface marker profile of human basophils and mast cells. In the present study, the characterization of these cell types was extended by the use of monoclonal antibodies (mAbs) to hemopoietic differentiation antigens. Basophils and mast cells were enriched by mAbs and complement from chronic myeloid leukemia blood (n = 5) and dispersed lung tissue (n = 4), respectively. A panel of 80 mAbs was tested for being reactive with purified cell populations using flow cytometry and/or a combined toluidine blue-immunofluorescence staining procedure. In addition to previous findings, basophils were found to react with mAbs directed against the 126-kilodalton dipeptidylpeptidase IV (CD26), platelet glycoprotein IIa (CD31), CD40 antigen known to share sequence homology with nerve growth factor receptor, leukosialin (CD43), CD44 antigen, the ICAM-1 antigen (CD54) and VIM2-reactive gangliosides involving the sialofucooligosaccharide sequence (CDw65L). Bsp-1 was found to be a specific marker for human basophils, whereas mast cells were not stained by this reagent. Basophils apparently lack CD22 antigen, gangliosides detected by CDw65 mAbs (except CDw65L) and CD71 antigen (transferrin receptor). Mast cells were found to express CD43 and CD44 antigen. In contrast, mast cells lack CD22, CD26, CD31, CD40 and CDw65 antigen. These results provide further evidence that both blood basophils and mast cells express a unique immunologic surface marker profile including binding sites for a variety of immunomodulating ligands and adhesion molecules.

Antibodies, Monoclonal↗
PubMed1995

Relationship between histamine release and leukotrienes production from human basophils derived from atopic dermatitis donors.

Basophils are known to release histamine and to produce leukotrienes (LTs) following both IgE-dependent and -independent stimuli. Although there exist a few reports which examined the relationship between histamine release and LTs production, their conclusions were not always in agreement with each other. In the present study, we examined the relationship between histamine release and LTs production from basophils in the presence or absence of 1 ng/ml of interleukin-3 (IL-3). Normal basophils released a smaller amount of histamine and LTs than atopic determatitis (AD) basophils, when basophils were stimulated with an optimal concentration of anti-IgE antibody. When we examined the relationship of histamine release and LTs production from AD donors induced through Fc epsilon RI, we found a significant exponential correlation between these two mediators (R2 = 0.58 in the absence of IL-3, R2 = 0.83 in the presence of IL-3). Although IL-3 enhanced both histamine release and LTs production from AD donors, the relationship between these two mediators was not affected. In conclusion, there was an exponential correlation between histamine release and LTs production from AD basophils, which was not affected by the pretreatment with IL-3.

Adolescent↗
PubMed1985

In vitro resistance to dexamethasone of basophils from patients receiving long-term steroid therapy.

Previous studies have shown that in vitro culture of human basophils for 24 h with physiologic concentrations of glucocorticoids leads to a pronounced inhibition of the subsequent release of histamine or leukotrienes when the cells are challenged with anti-IgE. However, both acute and chronic therapy in vivo with steroids fails to lead to an impairment of subsequent histamine release in vitro. To test whether the failure of in vivo steroid therapy to inhibit subsequent in vitro histamine release was due to the selection of a subpopulation of basophils that responded normally to anti-IgE but were resistant to steroids, the in vitro sensitivity to inhibition of mediator release by steroids in basophils obtained from normal patients as well as patients receiving chronic steroid therapy was studied. Basophils from steroid-dependent asthmatics (SDA) who had been receiving steroid doses orally of 7.5 to 50 mg equivalents of prednisone per day (mean, 19 mg), patients with collagen vascular disease (CVD) who had been receiving steroids orally of 4 to 80 mg equivalents (mean, 25 mg), non-steroid-dependent asthmatics (NSDA), and normal subjects were prepared, and their in vitro response to the potent glucocorticoid, dexamethasone, was determined. Dexamethasone was considerably more effective as an inhibitor of histamine release from basophils of normal subjects and NSDA than from basophils of SDA and patients with CVD. Because this was true in both SDA and patients with CVD, it seems most likely to be the result of the treatment with steroids rather than the underlying disease processes. Such a finding may be the result of a steroid-induced selection process by which sensitive cells are removed from the bloodstream in steroid-treated persons.

Adult↗
PubMed1987

A comparison of the osmotic activation of basophils and human lung mast cells.

Basophils and mast cells release histamine in hyperosmolar environments. Osmotic release differs significantly from IgE-dependent activation and may be important in the pathophysiology of anaphylactoid reactions during intravenous infusions of hyperosmolar radiocontrast dyes and of obstructive attacks suffered by asthmatics after exercise. To confirm reported differences in osmotic activation of basophils and lung mast cells, the process was compared systematically in the 2 cell types. Both cells were activated by hyperosmolar mannitol, glucose, sucrose, and NaCl, but histamine release from basophils rose sharply to a maximum at 1,050 mOsm/kg, whereas mast cells released maximally at 700 to 750 mOsm/kg. Release was partially Ca2+-dependent in basophils but was highly Ca2+-dependent in mast cells. Release in mast cells was rapid and essentially complete by 5 min, whereas 45 to 60 min were required in basophils. The temperature optimum in both cell types was 32 degrees C, and release in both was enhanced by drugs that increase intracellular cAMP (PGE2, IBMX, and db cAMP). We conclude that osmotic activation of basophils and mast cells is a nontoxic process that differs significantly from IgE-dependent histamine release. If it does indeed participate in the pathophysiology of human disease, different treatment strategies will be required to modulate this contribution.

Basophils↗