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At least 1,369 records · Page 76Linked to original sources
PubMed1992

Dust from carpeted and smooth floors. V. Cat (Fel d I) and mite (Der p I and Der f I) allergen levels in school dust. Demonstration of the basophil histamine release induced by dust from classrooms.

Sixty dust samples from schools in Norway were analysed for major allergens from cat and mite after sampling with the regularly used vacuum cleaners for 5 days and with a new model vacuum cleaner for 10 days, respectively. The major feline allergen Felis domesticus allergen I (Fel d I) was detected in all the classrooms, with ranges from 12 to 16,840 ng/m2 floor area. The mean Fel d I concentration was about 11 times higher per unit area carpeted floors as compared with smooth floors after the 10 days sampling period. Mite allergens Dermatophagoides pteronyssinus allergen I (Der p I) and Dermatophagoides farinae allergen I (Der f I) were detected in very low concentrations, with ranges from < 1 ng to 104 ng/m2 floor area. These findings suggest that the school is a protective environment against mite infestation, while the prevalence of cat allergens in classrooms seems higher than previously assumed. Basophil histamine release was measured after provocation with 20 dust extracts from 10 different schools. In nine of the 10 schools examined, the basophil histamine release caused by challenge with carpet dust was higher than the corresponding release with smooth floor dust. The calculated floor areas in each school in which dust led to 15% histamine release were from 2 to 55 times larger for smooth floors compared with carpeted floors. These results emphasize previous findings regarding higher allergen concentrations in classrooms with carpeted floors.

Allergens↗
PubMed1979

Functional relationship of macrophages and basophils to the thymus gland.

Human thymus epithelium, depleted of thymocytes and macrophages by means of organ culture, was used in chemotaxis experiments with peripheral blood cells. Such cultured thymus epithelium can attract specifically macrophages and basophils. T-lymphocytes were attracted only by short-term (8 day) cultured thymus tissue which still retains some of the original macrophage population. Thymic macrophages formed rosette structures with thymocytes. In other experiments 'activated' rabbit macrophages had the capability to destroy thymocytes, whether autochthonous or allogeneic. The possible role of macrophages and basophils in thymus function is discussed.

Animals↗
PubMed1984

Effects of enprofylline and theophylline on purified human basophils.

Extracts from purified human basophils revealed activity of cAMP-phosphodiesterase with a km-value of 0.59 microM. The enzyme was not activated by Ca-ions. Enprofylline and theophylline inhibited the enzyme in a competitive manner. Enprofylline was more potent than theophylline. These drugs did also inhibit the anti-IgE-induced histamine release from the basophils. These results favour the hypothesis that inhibition of histamine release of enprofylline is caused by an inhibition of phosphodiesterase. Although accumulating data have indicated that theophylline, at therapeutic concentrations, is a weak inhibitor of cAMP-phosphodiesterase activity, there is reason to believe that enprofylline, at therapeutic concentrations, may act at least partly as a phosphodiesterase inhibitor.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Clinical and immunological aspects of a case of monoclonal hyper-IgE. Isolation of IgE-protein, estimation of basophil cell bound IgE and histamine release.

A case of monoclonal IgE type lambda with IgE levels about 1 mg/ml has been followed for 6 years. Except for a slight asthma no signs of malignancies, parasitic infestations or other known diseases compatible with hyper-IgE have been found. By the combination of fractional ammonium sulphate precipitation, gel filtration, chromatofocusing, and subtraction affinity chromatography the IgE protein was isolated in an immunochemically pure and homogeneous form. Immunofluorescence of bone marrow cells showed about 1% IgE plasma cells. The amount of basophil bound IgE was 42 ng/10(6) cells, and histamine release from basophils challenged with anti-IgE was not different from that in atopic control persons, indicating a within-allergic-patients normal amount of IgE receptors. The protein-A reactivity was 0.4% equivalent to well-known IgE myeloma proteins. No antigen specificity of the IgE protein was found. Only a few cases of asymptomatic hyper-IgE are known, and it cannot be ruled out that this represents a premyeloma condition, since a similar case terminated in a malignant lymphoma.

Aged↗
PubMed1986

Influence of neuraminidase and N-acetylneuraminic acid on basophil histamine release in vitro.

Since N-acetylneuraminic acid (NANA) in cell membrane glucocalyx mediates or modulates a variety of actions, such as mediator release, we examined a possible modulating role of this amino sugar in histamine release from human basophil leukocytes. Removal of NANA from the cell membrane by the enzyme neuraminidase caused a dose-dependent histamine release. Removal of smaller amounts of NANA enhanced histamine release induced by anti-IgE, Concanavalin A and the calcium ionophore A23187, and reduced the interval between addition of antigen and initiation of histamine release. Pretreatment with free NANA had the opposite effects, i.e. a diminished and delayed maximal histamine release. The hypothesis that NANA in the cell membrane modulates the cellular response to stimulation was further substantiated by demonstrating that the altered response was reflected by a change in the sensitivity of the cell to extracellular calcium. NANA in the cell membrane glucocalyx thus seems to modulate the basophil response to stimulation by modulating transmembraneous calcium transport.

Adolescent↗
PubMed1986

Basophil histamine release in cord blood. Regulatory role of IgE.

Thirty-two cord blood samples were studied for histamine releasing capability by using a sensitive glass microfibre-based histamine analysis. Histamine was obtained after challenge with anti-IgE in 24 of the 32 samples. However, the net release in cord blood was only 25% of that in adult blood and no relationship was found between histamine release response, total IgE in cord plasma, and a family history of atopic diseases. The low histamine release in cord blood seemed to be associated with the immunological IgE receptor complex activation and not with an immature basic cell function, since the calcium ionophore A23187 which bypasses the receptor complex induced identical histamine release curves in cord and adult blood. Furthermore, when comparing the results of passive sensitization of basophils from new-born and adult persons, the new-born basophils possessed a significant fraction of free IgE receptors, whereas in adults most of the receptors were occupied by IgE.

Adult↗
PubMed1987

Fenoterol, a selective beta 2-adrenergic agonist, and inhibition of IgE-mediated basophil histamine release.

The present study was undertaken to evaluate the effect of fenoterol, a selective beta 2-adrenergic agonist, on basophil histamine release. Fenoterol at 10(-7) to 10(-3) M did not inhibit the release of histamine induced by Dermatophagoides farinae extract (D.f.) from leukocytes from allergic patients sensitive to mite. Similarly, there was no suppression of histamine release induced by anti-IgE and formyl-methionyl-leucyl-phenylalanine under the influence of fenoterol. Fenoterol caused a slight inhibition of the calcium ionophore A23187-induced histamine release at 10(-3) M with % inhibition of 11.8 +/- 2.4 (means +/- SEM, P less than 0.05). There was no synergism between fenoterol and theophylline in inhibiting D.f.-induced histamine release. Fenoterol did not suppress the release of histamine induced by antigen at low as well as high levels of release. Based on the data on the effect of fenoterol on IgE-mediated histamine release, it was concluded that in contrast to a human lung mast cell system, the beta-adrenergic receptor-adenylate cyclase system is not a control mechanism in IgE-mediated basophil histamine release.

Basophils↗
PubMed1987

Inhibition of basophil histamine release by gangliosides. Further studies on the significance of cell membrane sialic acid in the histamine release process.

Histamine release from human basophils was inhibited by preincubation of the cells with a glucolipid mixture containing sialic acid-containing gangliosides. This was true for histamine release induced by anti-IgE, Concanavalin A and the calcium ionophore A23187, whereas the release induced by S. aureus Wood 46 was not affected. It was demonstrated that the inhibitory capacity of the glucolipid mixture could be attributed to the content of gangliosides, since no inhibition was obtained with cerebrosides or with gangliosides from which sialic acid was removed. Preincubation of the cells with the glucolipid mixture increased the sialic acid content of the cells, and this increase was attributed to an insertion of gangliosides into the cell membrane. The inhibition of histamine release was abolished by increasing the calcium concentration, which substantiates our previous findings that cell membrane sialic acid in basophil leukocytes is involved in the regulation of histamine release, possibly by a modulation of the transmembraneous calcium fluxes preceding histamine release.

Basophils↗
PubMed1987

Effect of nitrendipine on histamine release from human basophil leukocytes.

The effect of the new calcium antagonist nitrendipine on in vitro basophil activation was evaluated in 10 subjects. The histamine release induced by calcium ionophore A23187, f-met peptide and anti-IgE was inhibited, in a dose-dependent fashion, by nitrendipine in the concentration range of 1-100 microM. The activity of this calcium antagonist seems complex and related to an interference with calcium at multiple sites. At concentrations higher than 200 microM, nitrendipine causes histamine release from basophil leukocytes. This histamine secretion is likely to be due to a cytotoxic effect, since it is associated with an increase in LDH levels in the cell supernatant.

Adult↗
PubMed1988

Role of protein kinase C in histamine release from human basophils.

In this study, we investigated the role of calcium and phospholipid-dependent protein kinase (protein kinase C, PKC) in the modulation of histamine release from human basophils. A novel and potent inhibitor of PKC, K-252a, inhibited the release of histamine induced by anti-IgE in a dose-dependent manner with ID50 (the dose required for 50% inhibition of histamine release) of 2.2 x 10(-8) M. Histamine release stimulated with 12-0-tetradecanoyl-phorbol-13-acetate(TPA) was also suppressed by K-252a with maximal inhibition of 48.0 +/- 9.3% at 10(-7) M. In contrast, K-252a did not inhibit the release of histamine in response to FMLP and ionophore A23187. Another inhibitor of PKC, H-7, exhibited a dose-dependent inhibition of anti-IgE-induced histamine release with ID50 of 8.6 x 10(-4) M. H-8 and HA1004, which closely resemble H-7 in chemical structure but are less potent in inhibiting PKC, did not inhibit histamine release stimulated with anti-IgE, but rather enhanced the release at higher concentrations. These results strongly suggest that PKC activation plays a crucial role in the mediation of IgE-mediated histamine release from human basophils.

Antibodies, Anti-Idiotypic↗
PubMed1988

Basophil histamine release in children with adverse reactions to cow milk. Comparison with RAST and skin prick test.

Basophil histamine release was examined in 26 children suspected of having cow milk allergy (CMA). Following oral challenge with cow milk, the initial adverse reaction reappeared in 20 children, the majority developing urticaria. The urticaria patients showed a high degree of correlation between the results of histamine test, RAST and skin test. Children with gastrointestinal symptoms reacted to milk challenge, but only a few showed a positive histamine test, RAST and skin test. Among the patients with atopic dermatitis, the tests gave mostly negative results, which was in accordance with the lack of response to a milk challenge. The results obtained by removal from and fixation to the cell surface of IgE indicate an IgE-mediated reaction in CMA, which, in connection with the correlation between histamine test and RAST or skin test, suggests basophil histamine release as a suitable method for testing Type I allergy in children suspected of CMA.

Animals↗
PubMed1989

Basophil histamine release and lymphocyte proliferation tests in latex contact urticaria. In vitro tests in latex contact urticaria.

Basophil histamine release and lymphocyte proliferation tests were examined with latex allergen prepared from surgical gloves in 15 patients with latex contact urticaria. The basophil histamine release test (BHRT) yielded positive results in 13/14 (93%) patients, whereas commercial latex RAST was positive in only 9/15 (60%) patients. Lymphocyte proliferation test (LPT) was positive in 3/15 (20%) patients, suggesting that cell-mediated immune reactions may also occur in latex allergy. However, patch tests to latex were negative and neither were epidermal Langerhans cells able to present latex antigen to T lymphocytes in vitro.

Adult↗
PubMed1989

Relevance of basophil histamine release changes during venom immunotherapy.

We investigated the effect of rush and long-term venom immunotherapy on histamine release parameters in bee venom allergic patients. Ten patients received rush venom immunotherapy, and histamine release data were obtained immediately before and after treatment. 17 patients were assessed by histamine release 24 to 63 months after termination of long-term venom immunotherapy. A control group of 10 non-allergic subjects was included in this study. Histamine released from whole blood was determined in a sensitive radio-enzymatic assay using a single isotope technique. Bee venom phospholipase A-induced histamine release from whole blood proved to be a test procedure of high specificity and sensitivity. Eight of 10 untreated patients and no control subject showed significant antigen-induced histamine release. Results obtained from patients immediately after successful rush venom immunotherapy showed an important decrease (mean 45.9%) of total histamine content of basophil leukocytes in all patients. Antigen-induced maximum histamine release was found to be increased in one, decreased in two and unchanged in seven patients. In patients who received long-term immunotherapy cell sensitivity to phospholipase A was significantly lower than in a group of untreated patients (P less than or equal to 0.002). These results suggest that even years after discontinuation of immunotherapy, histamine release parameters reflect patients' protection from systemic sting reactions as assessed by sting challenges. Histamine depletion of basophils induced by rush immunotherapy may play an important role in patients' protection immediately after termination of the rush regimen.

Adolescent↗
PubMed1990

Influenza A virus enhances basophil histamine release and the enhancement is abolished by carbohydrates.

Basophil histamine release was studied in leukocyte suspensions from normal individuals and from patients allergic to house dust mite or birch pollen. Mediator release caused by IgE-mediated reactions was examined by stimulating the cells with anti-IgE or specific antigens, and the calcium ionophore A23187 was used for a non-immunological histamine release. In all experiments influenza A virus caused a synergic enhancement of the mediator release and the potentiation was abolished by galactose (10(-7) to 10(-6) M) and by 10(-6) to 10(-5) M of N-acetylglucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. Wash-out experiments show that the sugars prevent the aggravation of mediator release by a binding of sugar to the basophil cell membrane, thereby causing a blockade of binding sites responsible for the potentiating effect of virus.

Adult↗
PubMed1991

Cutaneous and basophilic sensitivity to substance P and gastrin in non-atopic versus atopic subjects.

We compared the cutaneous reaction to intradermal injection of substance P, gastrin and histamine in asymptomatic atopic subjects with a history of hay fever and/or asthma versus non-atopic healthy volunteers. We also studied in these two groups the basophilic histamine release induced by substance P and gastrin with that obtained with anti-human IgE and Con A. Intradermal injection of substance P (3-300 pM) and gastrin (3-30 pM) caused a wheal and flare reaction which was comparable in both groups of subjects. Substance P 10(-4)M caused a mean basophilic histamine release of about 15% in atopic and non-atopic subjects. Gastrin was not effective in this model. Anti-IgE and Con A-induced histamine release was significantly higher in atopic than in non-atopic volunteers.

Adult↗
PubMed1991

Cytokine-induced histamine release from basophils of AIDS patients. Interaction between cytokines and specific IgE antibodies.

Basophil leukocytes obtained from AIDS patients, allergic patients and healthy controls were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8-17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig-dependent mechanism. Passive sensitization with cell-derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell-bound IgE was responsible for the cytokine-induced histamine release in AIDS patients. This response may be mediated by cytokine-selective IgE antibodies.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Virus, bacteria and lipopolysaccharide increase basophil cell response to histamine releasing stimulators and calcium. Examination of allergic and normal individuals.

Histamine release from human basophil leukocytes from allergic patients or controls was induced by specific antigens, anti-IgE or calcium ionophore A23187. Influenza A virus, S. aureus and lipopolysaccharide from S. typhimurium increased the maximum release of histamine and caused a shift to the left of the dose-response curves showing increased cell sensitivity and lowering of the threshold to these stimuli. The mechanism of action was elucidated by examining the mediator release as a function of increasing extracellular concentration of calcium. In these experiments the dose-response curves were changed by the microorganisms and lipopolysaccharide as before. This indicates that the microorganisms and lipopolysaccharide change the basophil cell response to IgE-dependent and non-immunological stimuli by causing a change in the subcellular handling of calcium.

Adult↗
PubMed1992

Assessment of histamine release from basophils in whole blood by benzylpenicilloyl poly-L-lysine in penicillin-sensitized patients.

Histamine release from basophil granulocytes in whole blood by benzylpenicilloyl poly-L-lysine (PPL) was investigated in 7 patients with penicillin allergy. All patients presented with systemic immediate hypersensitivity reactions after i.v. administration of penicillin G. Total histamine (of 7 patients) ranged from 27.5 ng/ml to 62.1 ng/ml (mean 43.2 ng/ml). The spontaneous histamine release ranged from 0.15% to 5.1% (mean 1.8%) of the total content. Addition of PPL in various concentrations resulted in values between 0.8 and 9.6%. Although PPL is a reliable allergen for prick- and intradermal testing in the diagnosis of penicillin allergy--demonstrating a histamine liberation in the skin--the in vitro experiment using the same allergen showed no histamine release above 10%. Using a threshold of 5% out of 7 patients, 4 (57%) would show a positive histamine release. Therefore it might indicate that in penicillin allergy a threshold of 5% must be used. In addition, basophils in whole blood and skin mast cells may be activated differently.

Adolescent↗