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PubMed1986

Peroxidase activity in circulating mast cells in blast crisis of chronic granulocytic leukemia. Comparative studies with basophils and cutaneous mast cells.

Although the hematopoietic origin of mast cells is very probable, the cell from which they originate is still a matter of speculation. The description of "transitional basophil/mast cells" in myeloproliferative disorders has suggested a common origin for basophils and mast cells. In a case of mast cell transformation of chronic granulocytic leukemia, the authors have studied the morphology and peroxidase activity by three classical technics, of circulating mast cells and transitional "basophil/mast cells." These results were compared with those of blood and bone marrow basophils and those of cutaneous mast cells. In both mast cells and "transitional basophil/mast cells," peroxidase activity was revealed in the nuclear envelope, endoplasmic reticulum, and granules. This activity was detected in unfixed cells and in tannic acid-aldehyde-fixed cells but not in 1.25% glutaraldehyde-fixed cells, where the staining appeared only in the granules. The comparison of this activity with that of normal basophils and mast cells suggests that the proliferating cells in this case possess at the same time the peroxidase activity of basophils and mast cells.

Aged↗

PubMed1987

A hybrid eosinophilic-basophilic granulocyte in chronic granulocytic leukemia.

Morphologic observation of the peripheral blood smear from a patient with chronic granulocytic leukemia suggested the presence of eosinophilic and basophilic granules in the same individual granulocyte. To unambiguously identify eosinophilic and basophilic granules simultaneously in the same preparation, the authors developed a cytochemical staining procedure using basophil-specific toluidine blue and eosinophil-specific cyanide-resistant peroxidase. Using this new dual stain, they demonstrated that ten out of ten chronic granulocytic leukemia patients they examined had cells that contained both eosinophilic and basophilic granules. The identity of the granules was corroborated by electron microscopic studies. These observations suggest that lineage confusion is common in chronic granulocytic leukemia.

Basophils↗

PubMed1997

Heterogeneous effects of protamine on human mast cells and basophils.

To investigate the mechanisms of anaphylactoid reactions to protamine, we have examined the in vitro effects of increasing concentrations of protamine (10(-6)-3 x 10(-4) mol litre-1) on the release of preformed (histamine and tryptase) and de novo synthesized (peptide leukotriene C4 (LTC4) or prostaglandin D2 (PGD2)) mediators from human basophils and mast cells isolated from lung parenchyma, heart, skin and synovial tissues. Protamine 10(-6)-3 x 10(-4) mol litre-1 induced release of histamine, but not de novo synthesis of LTC4 from basophils. At concentrations from 10(-5) to 3 x 10(-4) mol litre-1 it induced histamine release from human heart (mean 6.5 (SEM 1.5)%), skin (17.7 (4.1)%) and to a lesser extent from synovial mast cells, but not from lung mast cells. Protamine also caused the release of tryptase from heart mast cells (12.8 (3.2) micrograms/10(7) cells), but did not induce de novo synthesis of LTC4 and PGD2 from lung and skin mast cells. In these experiments cross-linking of IgE by anti-IgE caused release of LTC4 or PGD2 from human basophils or mast cells. These results demonstrate that protamine acted as an incomplete secretagogue, causing the release of preformed mediators from human basophils and mast cells.

Adult↗

PubMed1997

Monocyte chemotactic protein-1 is a proinflammatory chemokine in rat skin injection sites and chemoattracts basophilic granular cells.

Chemokines may control mast cell infiltrates found in many inflammatory diseases. These cells act through at least two main functions: migration and degranulation. Here we show that human recombinant monocyte chemotactic protein (MCP)-1 (10 ng/50 microliters) induces, after 4 h, an inflammatory vascular permeability and cellular extravasation reaction, determined by Evan's blue dye (1% in saline) injected into the tail vein of the rat, when injected intradermally in the rat skin. The blue color accumulating at the sites of injection provides evidence of vascular permeability and cellular extravasation. The colored areas of the skin were then enucleated and immersed in a fixative solution. Slides were prepared with sections of tissue colored with toluldine blue and analyzed under an optical microscope. A significant number of basophilic cells migrated to the injected area where MCP-1 (10 ng/50 microliters) was used compared to the control PBS treatment. Cell recruitment was slightly less than N-formyl-methionine-leucyl-phenylalanine (used at 10(-6) M/50 microliters). Electron microscopy studies confirmed the presence of basophilic granular cells where MCP-1 was intradermally injected. After preparation of a histidine decarboxylase (HDC) probe, a Northern blot analysis was determined for HDC mRNA in the enucleated tissue injected with MCP-1 (10 ng/50 microliters). Steady-state levels of HDC mRNA levels were induced after 4 h. These results were confirmed by the higher amount of histamine release, compared to the control PBS, in the enucleated tissue from the MCP-1 injection sites. Our results suggest that MCP-1 could play a significant role in diseases characterized by basophilic cell accumulation and migration to sites of tissue damage. Moreover, we show for the first time that MCP-1 is a pro-inflammatory chemokine that induces basophilic cell migration in rat skin injection sites.

Animals↗

PubMed1980

Basophilic transformation of chronic myelogenous leukemia.

Two patients with chronic myelogenous leukemia (CML) and basophilic transformation are reported because of unusual clinical and cutaneous features. One patient had the hyperhistaminemic syndrome (HHS) during relapse of the accelerated phase of CML. The literature on this topic is reviewed. The second patient had a basophilic crisis in the second year of CML. More than 100,000/cu mm basophils in the blood contrasted with infiltrates of eosinophils appearing in the skin and central nervous system. This striking cellular dichotomy suggested that the basophilic transformation of CML had acquired features mimicking the hypereosinophilic syndrome.

Basophils↗

PubMed1980

Cutaneous basophilic hypersensitivity response to fungal antigens in guinea pigs.

Guinea pigs infected with Trichophyton mentagrophytes developed a cutaneous fungal lesion and became skin test positive to fungal antigen (trichophytin). The cutaneous fungal lesion, while thought to be a cell-mediated response, differed histologically from the skin test site. Basophils were not demonstrated in biopsies of cutaneous fungal lesions, whereas basophils were numerous in biopsies of trichophytin skin test sites. When sensitization to trichophytin was accomplished by injection of hypha in complete Freund's adjuvant instead of infecting with live fungus, basophils could not be demonstrated in skin test sites. This report demonstrated that guinea pigs could be primed for cutaneous basophilic hypersensitivity (CBH) responses by infection with live fungus.

Animals↗

PubMed1988

In vitro immunological degranulation of human basophils is modulated by lung histamine and Apis mellifica.

1. The effect of high dilutions of two homeopathic drugs Lung histamine (Lung his) and Apis mellifica (Apis mel) used for the treatment of allergic diseases has been assessed on in vitro human basophil degranulation. Experiments were conducted blind. 2. Basophil degranulation induced by 1.66 X 10(-9) M anti-IgE antibody was significantly inhibited in the presence of 5 Lung his (5th centesimal dilution of Lung his) and 15 Lung his (15th centesimal dilution of Lung his) by 28.8% and 28.6% respectively and by 65.8% in the presence of 9 Apis mel (9th centesimal dilution of Apis mel). Basophil degranulation induced by 1.66 X 10(-16) to 1.66 X 10(-18) M anti-IgE antibody was also inhibited by high dilutions of Lung his and Apis mel with an inhibition of nearly 100% with 18 Lung his (18th centesimal dilution of Lung his) and 10 Apis mel (10th centesimal dilution of Apis mel). An alternance of inhibition, inactivity and stimulation was observed when basophils were incubated in the presence of serial dilutions of Lung his and Apis mel. 3. The investigation of the clinical efficacy of high dilutions of Lung his and Apis mel should be envisaged in allergic diseases in parallel with in vitro and ex vivo biological assays.

Animals↗

PubMed1981

Flow-cytometric analysis of human basophil degranulation. II. Degranulation induced by anti-IgE, anti-IgG4 and the calcium ionophore A23187.

Quantification of human basophil degranulation induced by anti-IgE, anti-IgG4, and by ionophore was performed using a flow-cytometric system. It was shown that these antibodies and ionophore can degranulate basophils in a dose-dependent manner, and that there is a wide variation in the response of basophils obtained from different individuals to these stimuli. A significant correlation was observed between the degree of degranulation induced by anti-IgE and anti-IgG4, while this was not the case for anti-IgE and ionophore. It was also shown that IgG4 myeloma protein can passively sensitive basophils. In general, degranulating efficacy was in the order of ionophore greater than anti-IgE greater than anti-IgG4, both in allergic and non-allergic individuals.

Anti-Bacterial Agents↗

PubMed1989

Inhibitory effect of terfenadine on mediator release from human blood basophils and eosinophils.

The effect of terfenadine on histamine release from human basophils and LTC4 production and release from human eosinophils was evaluated. Eosinophils and basophils were obtained by discontinuous gradient centrifugation of the peripheral blood of atopic asthma patients who were off medication. Anti-IgE-induced histamine release from human basophils was significantly inhibited by terfenadine. Maximum inhibition was obtained at 1 x 10(-5) M terfenadine (percentage inhibition = 57.0 +/- 20.1; P less than 0.05). However, only the highest dose of terfenadine used in this study, i.e. 2 x 10(-5) M, significantly inhibited calcium ionophore (A23187)-induced histamine release from human basophils (percentage inhibition = 40.0 +/- 14.6; P less than 0.05), and LTC4 production from human eosinophils (percentage inhibition = 59.8 +/- 9.9; P less than 0.05. These findings demonstrate that terfenadine, in addition to its known antihistamine property, also has an inhibitory effect on chemical mediator release.

Adolescent↗

PubMed1990

The inflammatory response in asthma exacerbation: changes in circulating eosinophils, basophils and their progenitors.

Circulating eosinophils, basophils and eosinophil/basophil (Eo/B) progenitors were examined in 12 patients at the time of an exacerbation of asthma accompanied by sputum eosinophilia and after resolution of the exacerbation with inhaled corticosteroid treatment. Differential counts were performed and peripheral blood non-adherent mononuclear cells were cultured for 14 days in methyl-cellulose to determine the number of Eo/B and granulocyte-macrophage (GM) colonies without knowledge of the clinical conditions or findings. With resolution of the asthma exacerbation on beclomethasone therapy, there were significant falls in circulating eosinophils, basophils and Eo/B colonies whereas GM colonies were unchanged. To elucidate whether the observed changes could be due to systemic absorption or local action of inhaled corticosteroid, seven subjects with allergic rhinitis and no current evidence of lower airway inflammation (no symptoms of asthma and normal methacholine airway responsiveness) received 14 days' treatment with the same dose of inhaled beclomethasone or of placebo in a double-blind randomized cross-over study. No significant changes in airway function or in circulating cell counts were observed. The results suggest reduced production of eosinophils and basophils after the resolution of an exacerbation of asthma. This effect may be due to reduced levels of airway-derived eosinophil-basophil growth and differentiation factors.

Adrenal Cortex Hormones↗

PubMed2004

Relevance of Ara h1, Ara h2 and Ara h3 in peanut-allergic patients, as determined by immunoglobulin E Western blotting, basophil-histamine release and intracutaneous testing: Ara h2 is the most important peanut allergen.

BACKGROUND: A number of allergenic proteins in peanut has been described and the relative importance of these allergens is yet to be determined. OBJECTIVES: We have investigated the relevance of previously identified peanut allergens in well-characterized peanut-allergic patients by in vitro, ex vivo and in vivo assays. METHODS: Thirty-two adult peanut-allergic patients were included based on careful and standardized patient history and the presence of peanut-specific IgE. The diagnosis peanut allergy was confirmed using double-blind placebo-controlled food challenges in 23 patients. Major peanut allergens Ara h1, Ara h2 and Ara h3 were purified from peanuts using ion-exchange chromatography. IgE immunoblotting was performed and IgE-cross-linking capacity was examined by measuring histamine release (HR) after incubating patient basophils as well as passively sensitized basophils with several dilutions of the allergens. Intracutaneous tests (ICTs) using 10-fold dilution steps of the purified allergens and crude peanut extract were performed. RESULTS: Ara h2 was recognized most frequently (26 out of 32) in all tests and induced both positive skin tests and basophil degranulation at low concentrations, whereas Ara h1 and Ara h3 were recognized less frequently and reacted only at 100-fold higher concentrations as analysed with HR and intracutaneous testing (ICT). Next to the three tested allergens, proteins with molecular weights of somewhat smaller than 15 kDa were identified as a IgE-binding proteins on immunoblot in the majority of the patients (20 out of 32). CONCLUSION: We conclude that Ara h2 is, for our patient group, the most important peanut allergen, and that previously unidentified peanut proteins with molecular weights of somewhat smaller than 15 kDa may be important allergens as well. ICT in combination with basophil-HR and IgE immunoblotting provides insight in the patient specificity towards the individual peanut allergens.

2S Albumins, Plant↗

PubMed2006

In contrast to specific B cells, human basophils are unaffected by the toxic activity of an allergen toxin due to lack of internalization of immunoglobulin E-bound allergen.

BACKGROUND: Specific immunotherapy is the only curative therapy for type I allergies and the alarming increase in allergy prevalence emphasizes the need for additional/alternative strategies for curative treatment. Allergen toxins (AT), fusion products of an allergen with an apoptosis inducing cytotoxin, are a new kind of immunotoxin. OBJECTIVE: AT should allow allergen-specific targeting and elimination of allergy-relevant cells, with B cells being the primary target. An important question is the fate of the effector cells, e.g. mast cells and basophils, which carry allergen-specific IgE: the immunotoxin might even prove to be harmful. METHODS: We established a reliable in vitro B cell model (using two mouse hybridoma cell lines) for testing specificity and toxicity of P5-ETA', a fusion protein of the major timothy grass pollen allergen Phl p 5b and truncated Pseudomonas Exotoxin A. In a second step, we investigated the impact of the AT on human basophils. RESULTS: P5-ETA' reliably eliminated Phl p 5-specific cells in the in vitro B cell model, leaving unspecific B cells unharmed. Human basophils of grass pollen allergic donors specifically bound P5-ETA', released IL-4 and up-regulated the activation marker CD203c, but were not subject to the toxic effect because of lack of internalization of IgE-bound allergen. CONCLUSION: According to our data, basophils are pure effector cells in the context of IgE-bound allergen and not involved in classical antigen presentation.

ADP Ribose Transferases↗

PubMed1996

Allergenic epitopes of ovalbumin (OVA) in patients with hen's egg allergy: inhibition of basophil histamine release by haptenic ovalbumin peptide.

We studied allergenic determinants that induce hypersensitivity to OVA, the major allergen in egg allergy, using immunoblot and histamine release assays. Immunoblot analysis demonstrated a part of the OVA epitope was in the C-terminal region comprising residues 347-385 (OVA347-385). Histamine was released from basophils of a patient with egg allergy upon stimulation with the OVA fragment corresponding to OVA347-385. Furthermore, detailed epitope mapping using overlapping peptides (residues 347-366, OVA-A; residues 357-376, OVA-B; and residues 367-385, OVA-C) in the OVA 347-385 region was carried out using the histamine release assay. In order for histamine release from basophils to occur, the allergen must possess two or more allergenic determinants located on the protein molecule at distances that would be equivalent to the distances between IgE molecules on the membrane surface. these results suggest that there are at least two epitopes that bind IgE antibodies on each OVA peptide. In addition, one epitope that binds IgE antibodies in two patients appears to reside in the haptenic peptide OVA357-366 (OVA-B1). The histamine release from basophils stimulated by OVA-B was completely inhibited by OVA-B1 in one of these patients. Similarly, OVA-B1 inhibited the histamine release produced by OVA-A in the other by more than 40%. These results suggest that haptenic synthetic peptides could regulate the allergic reaction in the effector phase if common epitope(s) recognized by IgE antibodies in the patients with egg allergy can be found. These are the first studies that provide an antigen-specific approach to inhibiting histamine release from basophils by a haptenic peptide recognized by IgE antibodies in an allergic disorder.

Allergens↗

PubMed1982

Progressive sensitization of circulating basophils against Ixodes ricinus L. antigens during repeated infestations of rabbits.

The sensitivity of rabbit basophils to antigens from Ixodes ricinus females has been studied by a degranulation test. Observations of basophil numbers and degranulation were made on the 6th day of each of four sequential infestations. Maximal degranulation of cells was observed after challenge of cells with antigen at a concentration of 10(6) and 10(7) pg/ml. At these concentrations, during a 1st infestation, 21.8 and 23.6% of cells degranulated. During a 2nd infestation, these percentages increased (34.8 and 33.8%) and reached 59.8 and 63.8% by the 4th infestation. A plasma factor which partially blocks basophil degranulation, is described. This was already present during the 1st infestation, since in its presence the percentage of degranulation was reduced by 2.8 and 4.0% respectively on challenge with 10(6) and 10(7) pg antigen/ml. Inhibition was maximal at the 4th infestation (difference: 16.5 and 20.5%). Basophil sensitization and inhibition of the degranulation are thus both progressive phenomena. After 10-15 infestations on four other rabbits, 75.0 and 79.8% degranulation was obtained. The inhibition of degranulation by plasma was also greater (difference: 25.5 and 27.4%). IgG specific anti-I. ricinus antibodies were identified by indirect immunofluorescence. In two animals, they were detected at the 6th day of the 1st infestation. Subsequently, they were generally present for all the animals.

Animals↗

PubMed1983

Role of phospholipase A2 activation in histamine release from human basophils.

The present experiments were undertaken to investigate the role of phospholipase A2 (PLA2) activation in histamine release from human basophils. A PLA2 inhibitor, P-bromophenacyl bromide (BPB), inhibited IgE-mediated anti-IgE-induced histamine release from human basophils with a concentration of drug required to produce 50% inhibition (IC50) of 1.5 x 10(-6) M when leukocytes were preincubated with this agent for 15 min. Histamine release induced by calcium ionophore A23187 and formyl-L-methionyl-L-leucyl-L-phenylalanine was also blocked by BPB with IC50 of 4.1 x 10(-6) M, and 3.5 x 10(-6) M, respectively. A PLA2 activator, 12-0-tetradecanoylphorbol-13-acetate (TPA) caused basophil histamine release with a dose-dependent fashion. BPB inhibited TPA-induced histamine release (IC50: 2.5 x 10(-6) M). However, another PLA2 activator, melittin, and PLA2 did not release histamine through non-cytotoxic mechanisms. Collectively, these results suggest that PLA2 activation plays a central role in histamine release from human basophils via generation of lysophosphatidylcholine or products of the lipoxygenase pathway of arachidonic acid metabolism.

Acetophenones↗

PubMed1991

Regulation of histamine release from human basophil leucocytes: role of H1, H2 and H3 receptors.

A novel class of histamine receptors (H3), controlling histamine synthesis and release, was described in rat and human brain and peripheral nerve endings. The present study was undertaken to evaluate whether H3 receptors contribute to the regulation of histamine release from human basophils. Basophil leucocytes were incubated with a H3 antagonist (thioperamide; concentrations ranging from 1 nM to 10 microM) or with a H3 ((R)alpha methyl-histamine; concentrations ranging from 1 to 100 mM), and subsequently were stimulated with optimal doses of anti-IgE and formyl-methionyl-leucyl-phenyl-alanine (f-met peptide). No significant modifications of histamine release were observed after incubation either with the H3 agonist or with the H3 antagonist. By contrast, a H2 antagonist (cimetidine; concentrations ranging from 1 to 100 microM) exerted a dose-dependent enhancing effect on anti-IgE- and, to a lesser extent, on f-met peptide-induced histamine release. A H1 antihistamine (chlorpheniramine; concentrations ranging from 100 nM to 1 microM), at the highest concentration employed, displayed an inhibitory activity on IgE-dependent and IgE-independent histamine release. Exogenous histamine was shown to exert a dose-dependent inhibitory effect on two-staged anti-IgE-induced histamine release. Taken as a whole, these results suggest that H3 receptors are not involved in the regulation of histamine release from human basophils; by contrast, H2 receptors participate in controlling histamine release from human basophils, as previously demonstrated by other authors.

Adult↗

PubMed1991

Delayed-type hypersensitivity and circulating basophils. A population study.

The factors related to delayed-type hypersensitivity (DTH) have been investigated in two samples of elderly non-hospitalized (n = 375) and hospitalized subjects (n = 409). Percent basophils was found to be consistently related to the number of positive responses to seven common antigens in the different samples or subsamples considered. The mean number of responses, after adjustment for age, sex and sample was 1.55 below 0.5% basophils, 1.87 between 0.5 and 1.5% and 1.96 over 1.5% (P less than 0.01). No relation was observed between percent basophils and the mean diameter of the positive responses, suggesting that basophils might be related to the early phase of DTH reactions. As previously reported, the number of positive responses was found to be lower in women than in men and to be inversely related to age.

Age Factors↗

PubMed1993

Investigation of basophil cell proteinase release in progressive systemic sclerosis.

The aim of this study was to evaluate the function of basophil granulocytes in 37 patients with progressive systemic sclerosis (PSS). The in vitro proteinase release test using Chromozyme TH as a chromogenic substrate was performed to measure the basophil cell releasability. Anti-IgE, calcium-ionophore (A 23187) and N-formyl-methyonil-leucyl-phenylalanine were used as activatory agents. Our results showed that the reactivity pattern to those agents did not differ in PSS compared to controls. Patients whose basophil cells release proteinases to all of the 3 activators tended to have more severe organ symptoms compared to the rest of the patients, while teleangiectasia was significantly less frequently (p < 0.02) found in cases with proteinase release. These findings suggest that there may be a certain relationship between basophil function and severity of the PSS.

Adult↗