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PubMed2003

Brown Norway rat ovalbumin-specific immunoglobulin E antibodies increase the human basophil expression of CD63 marker.

Anaphylactic shock is an immunoglobulin E (IgE)-dependent hypersensitivity. Biological tests like leucocyte histamine release (LHR) and human basophil activation (HBA), frequently used in human allergy, reflect both the amount of IgE fixed on cells and the cellular reactivity. To assess whether serum-specific IgE from Brown Norway (BN) rats prepared for ovalbumin (OVA)-induced anaphylactic shocks can activate human basophils which has a potential interest in experimental allergy: such a test could rapidly assert an IgE sensitization in laboratory animals genetically T-helper 2 (Th2)-predisposed. Rats (n = 39) were immunized three times (day 0, day 5 and day 21) with OVA injected subcutaneously. One week after the third immunization, a shock was induced with an intravenous (i.v.) bolus of OVA. Sensitization was assessed by passive cutaneous anaphylaxis (PCA) test and dosages of serum IgE antibodies anti-OVA by enzyme-linked immunosorbent assay. Blood basophils were counted before and during the shock. Before the shock induction (at day 21), an LHR test was performed on rat blood, and human basophils were sensitized with rat sera. HBA was demonstrated by the increase in the percentage of cells expressing CD63 antigen membrane, measured by flow cytometry. Twenty-one days after the first subcutaneous (s.c.) immunization, the rat serum induced a significant HBA. HBA was observed neither with the same serum previously heated nor with the serum from nonimmunized rats (NIRs). OVA-specific IgEs were significantly increased in immunized rat (IR) serum. The PCA test was negative when the serum was previously heated (56 degrees C). We never observed any circulating basophils, and LHR test was negative. After OVA i.v. administration, all IRs died rapidly. HBA testing strongly suggests a mediation by specific IgE in the increase of CD63 in BN rats. Thus, HBA test seems useful in assessing whether an experimental allergy was induced in animals genetically predisposed to an immune response, Th2-mediated, like BN rat. We also conclude that rat basophil activation does not participate in the histamine release during anaphylactic shock in sensitized BN rats.

Anaphylaxis↗
PubMed2000

Basophil and eosinophil accumulation and mast cell degranulation in the nasal mucosa of patients with hay fever after local allergen provocation.

BACKGROUND: Basophils and mast cells have certain similarities and are believed to be important in upper and lower respiratory allergy. OBJECTIVE: We sought to apply immunohistology to investigate the distribution and numbers of mast cells and basophils in the nasal mucosa after allergen provocation. METHODS: Allergen challenge with grass pollen was performed in 9 patients with seasonal allergic rhinitis out of the hay fever season. Nasal biopsy specimens were taken before and approximately 1 hour, 24 hours, and 1 week after intranasal allergen provocation. We determined relative numbers and their phenotypic characteristics by using mAbs specific for tryptase, chymase, IgE, eosinophils (BMK-13), and a new mAb against basophils (BB1) by using immunohistochemistry in frozen sections. RESULTS: In the nasal mucosa at baseline, practically no basophils were found in the epithelium. A significant increase in numbers was found in the epithelium and lamina propria of the nasal mucosa in the early phase as early as 1 hour after allergen provocation. At 24 hours and 1 week after allergen provocation, a significant increase in basophil numbers was found in the lamina propria only. The proportion of mast cells staining for chymase in the lamina propria decreased from a median of 38% (range, 0%-82%) to 14% (range, 0%-78%) within 1 hour of allergen provocation. The proportion of mast cells staining for chymase increased from 1% (range, 0%-86%) at baseline to 21% (range, 3%-85%) within 1 hour of allergen provocation. One week after provocation, mast cells returned to baseline numbers. A definite tissue eosinophilia was observed after allergen provocation. CONCLUSION: Basophil numbers are increased in the epithelium and lamina propria of the nasal mucosa of subjects with rhinitis after allergen challenge, with influx already apparent at 1 hour. Moreover, changes in mast cell percentages and numbers were observed within 1 hour of allergen provocation.

Adult↗
PubMed2001

Mechanisms of autoimmune activation of basophils in chronic urticaria.

BACKGROUND: Approximately 35% to 40% of patients with chronic urticaria possess a circulating antibody directed to the alpha subunit of the high-affinity type I IgE receptor (FcepsilonRI), which is detectable by using histamine release assays or immunoblotting. Prior reports suggest that purified IgG may not directly activate basophils but rather does so through complement activation. OBJECTIVE: We sought to further elucidate the mechanism by which this antibody causes basophil histamine release, including the role of complement, and to reassess the relationship of functional versus binding assays. METHODS: We incubated human basophils with patient serum, patient IgG, or patient IgG plus normal serum as a complement source and measured histamine release for each condition. IgG fractions were neutralized with cloned alpha subunit to determine whether histamine release decreased proportionately. We also screened sera from 260 patients to compare histamine release with immunoblotting results. RESULTS: We initially tested 35 sera from patients with chronic urticaria by using basophils from 2 atopic donors and one nonreleaser with rabbit anti-IgE. No histamine was released from the nonreleaser, yet all donors responded identically to monocyte chemotactic protein 1, indicating a requirement for IgE or the IgE receptor. Basophil histamine release was markedly augmented by complement if release by IgG alone was low. Incubation of purified IgG with an increasing concentration of cloned alpha subunit gradually reduced the histamine-releasing capability in patients with positive or negative immunoblot results. Of 260 patients tested, 43% had positive histamine release results, and 47% had positive immunoblot results, yet there was no correlation when individual patients were assessed. CONCLUSION: A subpopulation of patients with chronic urticaria possess IgG antibody directed to the alpha subunit of FcepsilonRI. This IgG activates basophils, which is dependent on or augmented by complement. Binding assays for the FcepsilonRI alpha subunit, such as immunoblotting, are not currently feasible as a screening method. A functional assay is required.

Autoantibodies↗
PubMed2002

Characterization of mast-cell tryptase-expressing peripheral blood cells as basophils.

BACKGROUND: Mast-cell tryptase is a protease with proinflammatory activity, the expression of which by peripheral blood leukocytes (PBLs) has not been fully characterized. OBJECTIVE: We examined tryptase expression in human PBLs to further characterize this tryptase-expressing cell population for lineage and disease association. METHODS: PBLs were fixed, permeabilized, stained with antibodies to tryptase and a panel of mast cell- and basophil-specific markers, and analyzed by means of flow cytometry. RESULTS: Tryptase expression was restricted to a population of cells that stained positive for IgE and negative for the panel of lineage markers (IgE(+), lin(-)). This IgE(+), lin(-) population did not stain for the mast-cell markers Kit or chymase but did stain for the basophil-specific granule proteins recognized by the 2D7 and BB1 mAbs. Per-cell tryptase expression demonstrated a greater than 100-fold range of expression among donors but did not correlate with disease status (asthma or mastocytosis), FEV(1), or serum tryptase concentration. Tryptase was released by purified basophils after anti-IgE activation. CONCLUSIONS: The phenotype of tryptase-expressing PBLs and their lack of increase in patients with mastocytosis demonstrates that these cells are basophils. Per-cell basophil tryptase expression is highly variable between donors, with some donors expressing levels approaching those of mast cells. As such, anti-tryptase antibodies cannot be used to distinguish these 2 cell types from one another by means of flow cytometry. These results demonstrate that tryptase represents an additional mediator through which basophils may contribute to allergic inflammation.

Asthma↗
PubMed2002

Retinoic acid modulates IL-5 receptor expression and selectively inhibits eosinophil-basophil differentiation of hemopoietic progenitor cells.

BACKGROUND: IL-5 plays a central role in eosinophil and basophil differentiation, exerting its effects through the IL-5 receptor (IL-5Ralpha). Currently, little is known concerning regulation of IL-5Ralpha expression in the context of commitment of hemopoietic progenitor cells to the eosinophil and basophil lineages. OBJECTIVE: Because all-trans retinoic acid (ATRA) is known to modulate some aspects of hemopoietic differentiation, we examined the effects of ATRA on eosinophil-basophil differentiation and IL-5Ralpha expression. METHODS: Progenitor cells were obtained from bone marrow aspirates and cord blood samples. Enriched populations of CD34(+) cells were isolated by means of positive immunomagnetic selection with MACS beads. RESULTS: In semisolid methylcellulose cultures of normal human bone marrow, ATRA (10(-6) mol/L) selectively suppressed eosinophil-basophil colony-forming units but had no effect on granulocyte-macrophage colony-forming units. Similarly, ATRA (10(-6) mol/L) inhibited eosinophil-basophil differentiation of cord blood CD34(+) cells in liquid culture, whereas neutrophil differentiation proceeded without impediment. Most importantly, these effects of ATRA (10(-8) to 10(-6) mol/L) on CD34(+) cells were associated with a dose-dependent inhibition of IL-5Ralpha but no change in GM-CSF receptor expression, as detected with flow cytometry. CONCLUSIONS: These findings indicate that retinoids can differentially regulate expression of IL-5Ralpha, but not GM-CSF receptor, and that these effects have functional consequences in vitro on eosinophil and basophil differentiation.

Antigens, CD34↗
PubMed1971

Electron microscopic localization of immunoglobulin E on the surface membrane of human basophils.

We have examined human leukocyte preparations for the presence of surface-bound IgE by electron microscopy. Basophil-enriched leukocytes were reacted with burro anti-IgE, a hybrid antibody to burro IgG and ferritin, and ferritin, with or without prior incubation of the cells with an IgE myeloma protein. In the absence of preincubation with IgE small amounts of ferritin were fixed to the surface of basophils but on no other cells. When cells were preincubated with IgE the amount of ferritin fixation on the basophils was markedly increased and a small amount of ferritin was also bound to platelets but again to no other leukocytes. The distribution of ferritin on the basophil surface appeared dependent upon the temperature at which the cells were kept during and after reaction with the various reagents. Basophil sections from cells kept at 0 degrees C had ferritin bound to the surface membrane in patches distributed around the entire circumference. Basophil sections from cells prepared at room temperature had ferritin distributed assymetrically covering a surface membrane segment one-fifth to one-half of the circumference. In control studies in which monomeric IgG was substituted for the IgE and burro anti-IgG was used instead of burro anti-IgE, no cellular fixation of ferritin was observed.

Animals↗
PubMed1973

Cutaneous basophil hypersensitivity in contact-sensitized guinea pigs. I. Transfer with immune serum.

Cutaneous basophil hypersensitivity, an immune inflammatory reaction characterized by infiltrates of basophils and a delayed time-course, was studied in guinea pigs contact sensitized with oxazolone. Routine histological techniques, employing ordinary paraffin sections, were modified to study this reaction. When biopsies of contact lesions were processed by these methods dense infiltrates of basophils could be demonstrated. Animals sensitized with complete Freund's adjuvant emulsified with oxazolone-keyhole limpet hemocyanin conjugates also developed delayed-in-time responses to contact challenge with oxazolone but not to picryl chloride. These hapten-specific delayed-in-time reactions also contained substantial numbers of basophils. Transfer of serum from actively sensitized guinea pigs resulted in specific accumulation of basophils at challenge sites of recipients. Thus, in this experimental system, cutaneous basophil hypersensitivity was found to be a hapten-specific delayed-in-time reaction that could be transferred with immune serum.

Adjuvants, Immunologic↗
PubMed1983

Factor-dependent in vitro growth of human normal bone marrow-derived basophil-like cells.

A factor(s) present in supernatants from lectin-stimulated peripheral blood mononuclear cells promoted the production of basophil-like cells in liquid cultures of normal human bone marrow cells. The cultured basophil-like cells had lobulated or round nuclei, and the cytoplasmic granules stained metachromatically with toluidine blue and azurophilic with Giemsa. 20% of the metachromatically staining cells were peroxidase positive but not positive for nonspecific esterase. The histamine content was 0.5-2 pg/cell. The basophil-like cells released histamine upon challenge with calcium ionophore A23187 but not with compound 48/80. They also released histamine with anti-IgE when passively sensitized with human myeloma IgE. The development of basophil-like cells was promoted in a dose-dependent fashion by a factor(s) in the conditioned medium. Blocking of cell proliferation with hydroxyurea or X irradiation inhibited the development of basophil-like cells. The production of the factor was dependent on the presence of T cells. The factor was different from interleukin 2 and its molecular weight was estimated to be 25,000-40,000 by gel filtration on a Sephacryl S-200 column. Thus, human basophil-like cells derived from normal bone marrow cells can grow and differentiate in vitro under the regulation of T cells.

Basophils↗
PubMed1991

Adhesion of human basophils, eosinophils, and neutrophils to interleukin 1-activated human vascular endothelial cells: contributions of endothelial cell adhesion molecules.

Cytokines such as interleukin 1 (IL-1) promote adhesiveness in human umbilical vein endothelial cells for leukocytes including basophils, eosinophils, and neutrophils, and induce expression of adherence molecules including ICAM-1 (intercellular adhesion molecule-1), ELAM-1 (endothelial-leukocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1). In the present study, blocking monoclonal antibodies (mAb) recognizing ICAM-1, ELAM-1, and VCAM-1 have been used to compare their roles in IL-1-induced adhesion of human basophils, eosinophils, and neutrophils. IL-1 treatment of endothelial cell monolayers for 4 hours induced a four- to eight-fold increase in adhesion for each cell type. Treatment of endothelial cells with either anti-ICAM-1 or anti-ELAM-1 mAb inhibited IL-1-induced adherence of each cell type. In contrast, treatment with anti-VCAM-1 mAb inhibited basophil and eosinophil (but not neutrophil) adhesion, and was especially effective in blocking eosinophil adhesion. The effects of these mAb were at least additive. Indirect immunofluorescence and flow cytometry demonstrated expression of VLA-4 alpha (very late activation antigen-4 alpha, a counter-receptor for VCAM-1) on eosinophils and basophils but not on neutrophils. These data document distinct roles for ICAM-1, ELAM-1, and VCAM-1 during basophil, eosinophil, and neutrophil adhesion in vitro, and suggest a novel mechanism for the recruitment of eosinophils and basophils to sites of inflammation in vivo.

Antibodies, Monoclonal↗
PubMed1992

Monocyte chemotactic protein 1 is a potent activator of human basophils.

Cytokines belonging to the RANTES/SIS family are highly induced in a number of pathophysiological processes such as autoimmune disorders, cancers, atherosclerosis, and chronic inflammation. However, apart from their chemotactic activity on monocytes and particular lymphocyte types, the biological activities in the human system of this recently discovered cytokine family are largely unknown. Here we report that one family member, described as monocyte chemotactic protein 1 (MCP-1), strongly activates mature human basophils in a pertussis toxin-sensitive manner. MCP-1 causes a rise in the cytosolic free calcium level in basophils and monocytes, but not in other blood leukocyte types, and triggers basophil degranulation at low concentrations (ED50 = 3-10 nM). Thus, MCP-1 is a cytokine capable of directly inducing histamine release by basophils. Furthermore, MCP-1 promotes the formation of leukotriene C4 by basophils pretreated with interleukin 3 (IL-3), IL-5, or granulocyte/macrophage colony-stimulating factor. MCP-1-induced basophil mediator release may play an important role in allergic inflammation and other pathologies expressing MCP-1.

Basophils↗
PubMed1996

Deletion of the NH2-terminal residue converts monocyte chemotactic protein 1 from an activator of basophil mediator release to an eosinophil chemoattractant.

Chemotactic cytokines of the CC subfamily (CC chemokines) are considered as major mediators of allergic inflammation owing their actions on basophil and eosinophil leukocytes. The monocyte chemotactic protein (MCP) 1 is a potent inducer of mediator release from basophils but is inactive on eosinophils. To obtain information on the structural determinants of the activities of MCP-1, we have synthesized several NH2-terminally truncated analogues and tested their effects on basophils and eosinophils. Through deletion of the NH2-terminal residue, MCP-1(2-76) was obtained, which was a potent activator of eosinophils, as assessed by chemotaxis, cytosolic free Ca2+ changes, actin polymerization, and that induction of the respiratory burst. In contrast, the activity of MCP-1(2-76) on basophil leukocytes was dramatically decreased (50-fold) compared with that of full-length MCP-1. Deletion of the next residue led to total loss of activity on eosinophil and basophil leukocytes. Analogues with three or four residue deletions, MCP-1(4-76) and MCP-1(5-76), were again active on both cells, whereas all further truncation analogues, MCP-1(6-76) through MCP-1(10-76), were inactive. Thus, a minimal structural modification can change receptor and target cell selectivity of MCP-1. Our observations indicate that the recognition sites of CC chemokine receptors on eosinophils and basophils are similar, although they discriminate between MCP-1 and MCP-1(2-76) and suggest NH2-terminal processing as a potential mechanism for the regulation of CC chemokine activities.

Actins↗
PubMed1996

IL-4 production by allergen-stimulated primary cultures: identification of basophils as the major IL-4-producing cell type.

As a potent inducing agent for IgE production and differentiation factor for allergen-specific Th2 cells, IL-4 is a key regulatory cytokine both in the pathogenesis of allergic disease and in the ongoing allergic response. The assay of in vitro IL-4 production has often been used to compare the allergen responses of T cells isolated from atopic and non-atopic subjects. Because peripheral blood basophils also have the capacity to respond to specific allergen by producing IL-4, we investigated the relative contribution of these two cell types to IL-4 production in allergen-stimulated primary cultures. Among unfractionated peripheral blood mononuclear cells (PBMC), the major producers of detectable IL-4 in primary in vitro cultures were found to be basophils based on: (i) an allergen dose-response corresponding closely to that required for basophil histamine release and lower than that required for T cell activation; (ii) a rapid time course for IL-4 production (detectable at 3 h), inconsistent with the typical activation requirements of fresh T cells; (iii) the production of comparable levels of IL-4 in cultures stimulated with allergen or anti-IgE; and (iv) the complete loss of detectable IL-4 production following specific depletion of basophils from PBMC. The T cells in these cultures were functionally able to produce IL-4, as demonstrated by mitogen activation of basophil-depleted PBMC. These findings demonstrate that although IL-4 production in primary in vitro cultures can be used as a sensitive indicator of allergen responsiveness, the accurate interpretation of this result requires identification of the responding cell type. Furthermore, these findings raise the possibility that basophil production of IL-4 early in the course of allergen stimulation may shape subsequent T cell responses both in vivo and in vitro.

Allergens↗
PubMed1980

Evidence of sensitized basophils in renal transplanted patients.

The participation of basophil polymorphonuclear leukocytes in the response to kidney allografts in man has hardly been studied. In 23 patients, followed from the immediate post-transplant period for several years, the number of circulating basophils, expressed either as absolute number or as percentage of leukocytes, was significantly low in relation to that of controls. IgE on the basophil surface was determined by radioimmunoassay in 14 patients. All patients but one had elevated numbers of IgE molecules per basophil, values being higher in patients with cadaver grafts and in patients with a graft functioning at 6 months or less. When the count of circulating basophils was roughly normal, six of the eight patients showed a positive basophil degranulation test against the donor lymphocytes. These results suggest the existence of specific IgE antibodies for HLA antigens in renal transplanted patients.

Basophils↗
PubMed1987

Ultrastructural cytochemistry of congenital basophilic leukemia.

A newborn infant was diagnosed as having congenital basophilic leukemia, an extremely rare disorder, by examination of cord blood. An ultrastructural cytochemical study was conducted on the blasts of the infant. Granules of basophil blasts showed ultrastructural characteristics of immature basophil granules and were similar in size to those of normal basophil granules but were fewer in number in each profile. Histochemical studies showed weak reactions for acid mucopolysaccharides and neutral glycoconjugates in the granules, but they were negative for peroxidase. Acid phosphatase was markedly positive. The findings of congenital basophilic leukemia are different from those of basophils in chronic myelocytic leukemia. The patient underwent induction therapy with vincristine and prednisone and has been in complete remission for 21 months.

Basophils↗
PubMed1989

IgG anti-IgE from atopic dermatitis induces mediator release from basophils and mast cells.

IgG antibodies containing anti-IgE activity isolated from a patient with atopic dermatitis (H-aIgE) induced mediator release from human basophils and mast cells isolated from skin and lung tissues. The release of histamine was calcium- and temperature-dependent and did not involve cytotoxicity. There was an excellent correlation (r = 0.88; p less than 0.001) between the maximum percent histamine release from human basophils induced by rabbit anti-IgE (R-aIgE) and H-aIgE. H-aIgE was approximately 30 times more potent than R-aIgE in inducing mediator release from human basophils, skin, and lung mast cells. H-aIgE specifically desensitized human basophils to a subsequent challenge with both H-aIgE and R-aIgE. Lactic acid removal of IgE from human basophils blocked the releasing activity of both R-aIgE and H-aIgE. Passive sensitization with hyperimmune sera or purified IgE myeloma restored the response of basophils to both R-aIgE and H-aIgE. IgE purified from three different myeloma patients concentration-dependently blocked the histamine releasing activity of both R-aIgE and H-aIgE.

Adolescent↗
PubMed1991

Characterization of leukaemic basophil progenitors from chronic myelogenous leukaemia.

We describe the unique characteristics of leukaemic basophils from a patient with chronic myelogenous leukaemia (CML). The leukaemic cells were immature basophil-like blasts and expressed CD4, CD7 and HLA-DR in addition to CD13 and CD33. Both immunoglobulin and T cell receptor genes were retained in germline configurations. Interleukin-1 (IL-1) or granulocyte-macrophage colony-stimulating factor (GM-CSF) as well as IL-3 or IL-4 enhanced the proliferation and differentiation of leukaemic cells and only basophils were generated from in vitro culture. These results suggest that basophil progenitors expressing CD4, CD7 and HLA-DR may be involved in the development of basophilic crisis of CML and that both IL-1 and GM-CSF may act on basophil progenitors as well as IL-3 or IL-4.

Antigens, CD↗
PubMed1992

Haemopoietic growth factors induce human basophil migration in vitro.

Accumulation of basophils in inflammatory sites is an important aspect of the late-phase allergic reaction involving skin and upper and lower airways, suggesting the existence of mechanisms for basophil migration. Because haemopoietic growth factors have been shown to stimulate various functions of human basophils, we tested the ability of haemopoietic growth factors to migrate basophils in vitro. Both IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) induced migration of purified normal basophils (purity c. 80%) in a dose-dependent fashion at picomolar concentrations, while granulocyte (G)-CSF, macrophage (M)-CSF, and IL-4 had no effect at all. Chequerboard analyses indicate that migratory activity of both factors are chemokinetic. These results suggest that local production of both factors during allergic reactions might potentially play an initial role in the recruitment of basophils from the circulation to sites of inflammatory reactions.

Antibodies↗
PubMed2005

Functional analysis of cross-reactive immunoglobulin E antibodies: peanut-specific immunoglobulin E sensitizes basophils to tree nut allergens.

BACKGROUND: Peanut and tree nuts are a major cause of food-induced anaphylaxis with an appreciable mortality. Co-sensitization to peanuts and tree nuts is a common clinical observation and may be because of peanut-specific serum IgE antibodies that cross-react with tree nut allergens. It is, however, unclear whether these cross-reactive IgE antibodies are involved in effector-cell activation. OBJECTIVE: To determine if cross-reactivity of peanut-specific IgE antibodies with tree nuts can cause effector cell activation using an in vitro basophil activation assay. METHODS: Two peanut allergic subjects with positive specific IgE for peanut and tree nuts (as measured by CAP-FEIA) were studied. Basophil activation to peanut and tree nuts, as indicated by CD63 expression, was assessed by flow cytometry to confirm co-sensitization to peanut and tree nuts. Inhibition ELISA using sera from the subjects was performed to detect peanut-specific IgE antibodies that cross-reacted with tree nut proteins. To determine whether cross-reactive tree nut allergens can induce effector-cell activation, peanut-specific antibodies were affinity purified from the subject sera and used to resensitize non-peanut/tree nut allergic donor basophils stripped of surface IgE. Basophil activation was then measured following stimulation with peanut and tree nut extracts. RESULTS: The two peanut allergic subjects in this study showed positive basophil activation to the peanut and tree nut extracts. Inhibition ELISA demonstrated that pre-incubation of the peanut allergic subject sera with almond, Brazil nut and hazelnut extracts inhibited IgE binding to peanut extract. IgE-stripped basophils from non-peanut/tree nut allergic subjects resensitized with affinity-purified peanut-specific antibodies from the peanut allergic subject sera became activated following stimulation with peanut, almond and Brazil nut extracts, demonstrating biological activity of cross-reactive IgE antibodies. CONCLUSION: Peanut-specific IgE antibodies that cross-react with tree nut allergens can cause effector-cell activation and may contribute to the manifestation of tree nut allergy in peanut allergic subjects.

Adolescent↗