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  • 1
    Electronic Resource
    Electronic Resource
    Cytokine-induced release of histamine from basophil leukocytes from AIDS patients (1990)
    Springer
    Inflammation research 30 (1990), S. 294-296 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cytokine-induced histamine release from basophil leukocytes was examined in cell suspension from AIDS patients and compared with healthy controls. Cells from approximately half of the AIDS patients, in contrast to none from the control group, showed histamine release after stimulation with interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), lymphotoxin (LT) and interferon gamma (IFN gamma). These cytokines seem to induce histamine release from cells from AIDS patients by interaction with the cell surface immunoglobulins, since removal of the immunoglobulins prior to the exposure of the cytokines completely abolished the response to the cytokines. IL-1 alpha, IL-1 beta, IL-3, colony stimulating factor (CSF) and granulocyte-macrophage-CSF (GM-CSF) caused significant histamine release from cells from a similar number of AIDS patients and controls.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01969065
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  • 2
    Electronic Resource
    Electronic Resource
    Measurement of histamine release from human lung tissue ex vivo by microdialysis technique (1998)
    Springer
    Inflammation research 47 (1998), S. 501-505 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Microdialysis — Lung mast cells — Histamine release — Anti-IgE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: Currently no method is available for measurement of mediator release from intact human lung. In this study, a microdialysis technique was used to measure histamine release from mast cells in human lung tissue ex vivo.¶Material: Microdialysis fibers of 216 μm were inserted into lung tissue and perfused with Krebs Ringer buffer at a rate of 3 μl/min. After a 15 min period of steady-state perfusion, anti-IgE and vehicle were injected into the lung tissue above individual fibers. Samples from each fibre were collected for 20 min at 2 min intervals. Histamine was assayed fluorometrically.¶Results: Anti-IgE concentrations of 40–40,000 U/ml dose-dependently released histamine, significant histamine release being demonstrated with anti-IgE concentrations of 400 U/ml and greater. The kinetics of histamine release showed peak values 2–8 min after the injection. Great individual responses were observed but data could be reproduced within individual donors. Monocyte chemoattractant protein-1, a potent basophil secretagogue, did not induce histamine release in lung tissue which indicated mast cells to be the histamine source. Substance P did not release histamine in the lung tissue.¶Conclusions: The microdialysis technique allowed measurements of histamine release from mast cells in intact lung ex vivo. The method may prove useful since a number of experiments can be performed in a few hours in intact lung tissue without any dispersion or enzymatic treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050365
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  • 3
    Electronic Resource
    Electronic Resource
    Increased numbers of circulating basophils with decreased releasability after administration of rhG-CSF to allergic patients (1994)
    Springer
    Inflammation research 41 (1994), S. C24 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Preliminary studies in hematological patients have indicated that treatment with rhG-CSF reduces basophil releasabilityex vivo. We examined this phenomenon further, in allergic patients. Ten patients with grass pollen rhinoconjunctivitis were given rhG-CSF (5 μg/kg/day s.c.) for 5 days, and examined before and after treatment. Basophil counts increased from 5 to 19×109/l (P〈0.01). Total blood histamine increased from 80 to 160 μg/l (P〈0.01), corresponding to a decrease in average basophil histamine content from 1.5 to 0.81 pg/cell (P〈0.01). Isolated mononuclear cells showed a significantly decreased histamine release (HR) when stimulated with A23187 and grass. Whole blood experiments showed a similar decreased HR to grass and anti-IgE (P〈0.01). However, we found an increase in total blood histamine. We conclude that treatment with rhG-CSF (1) increases the number of circulating blood basophils, (2) reduces the average histamine content per basophil, and (3) reduces the basophil releasability. These findings could be due to the mobilization of immature basophils from the bone marrow.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02007750
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  • 4
    Electronic Resource
    Electronic Resource
    Bacteria-induced IgE-mediated histamine release: Examination of patients with chronic bronchitis (CB) during acute exacerbations (1994)
    Springer
    Inflammation research 41 (1994), S. C22 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Twelve patients hospitalized with acute exacerbations of chronic bronchitis (CB) and infected in the lower respiratory tract withH. influenzae (HI) orStreptococcus pneumoniae (SP) were examined. Bacteria, isolated from the expectorate caused an IgE-mediated histamine release from the patient's own blood leukocytes, indicating that all were sensitized to their own bacteria. Sensitization was only observed in some of the patients when tested with a standard panel of HI or SP obtained from other patients, indicating the importance of using the patient relevant bacterial antigenic determinants. No sensitization was found in twelve controls. The patients showed cellular hyperreactivity to HI and SP, i.e. the releasability was higher than in the control group. The cellular hypereactivity was not dependent on sensitization since it was also found against the non-infecting species. Both sensitization and cellular hyperreactivity may contribute to the aggravation of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02007749
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  • 5
    Electronic Resource
    Electronic Resource
    IgE-mediated immune response to Helicobacter pylori examined by basophil histamine release in patients with dyspepsia (2000)
    Springer
    Inflammation research 49 (2000), S. 29-30 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00000168
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  • 6
    Electronic Resource
    Electronic Resource
    Chlamydia pneumoniae and chronic obstructive pulmonary disease: bronchial biopsies (PCR and culture) and specific serum antibodies in patients and controls (2000)
    Springer
    Inflammation research 49 (2000), S. 37-38 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00000172
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  • 7
    Electronic Resource
    Electronic Resource
    HIV antigen stimulates basophil leukocytes from AIDS patients to release histamine due to type I allergy (1989)
    Springer
    Inflammation research 27 (1989), S. 55-57 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract HIV antigen-induced histamine release was examined in leukocyte suspensions from 12 patients with AIDS and 10 healthy controls. Nine of the twelve patients released histamine, while no release was obtained in cells from the control group. The mechanism was examined by removal of immunoglobulins (Ig) from the patient cells before stimulation with HIV antigen, which resulted in an abolition of the histamine release. Transfer of the Ig to cells from normal individuals rendered these cells able to respond to HIV. The removal and fixation of Ig were followed by disappearance and reappearance of the response to anti-IgE. These findings indicate that the histamine release by HIV is caused by a type I (IgE-mediated) reaction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02222197
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  • 8
    Electronic Resource
    Electronic Resource
    Staphylococcus aureus and influenza A virus stimulate human bronchoalveolar cells to release histamine and leukotrienes (1989)
    Springer
    Inflammation research 27 (1989), S. 107-109 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mediator release was examined from superficially lying cells in the airway epithelium obtained by bronchoalveolar lavage (BAL) in 13 non-atopic individuals. The BAL-cells were incubated (20 min, 37°C) withStaphylococcus (Staph.) aureus or with human influenza A virus.Staph. aureus was found to release histamine from cells from 7 of the 13 individuals and influenza A virus in 3 of 5 persons. Furthermore,Staph. aureus stimulated the BAL-cells to release leukotriene B4 in 7 of 11 subjects, whereas no release was found by influenza A virus in 7 examined persons. When cells from 4 persons were stimulated withStaph. aureus no release of leukotriene C4 was found. The mediator release caused by bacteria and virus might be of importance for the exacerbation of bronchial asthma in upper respiratory tract infections, since histamine is assumed to increase the epithelial permeability with entrance of allergens and other insulting particles, and leukotriene B4 facilitates airway inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02222212
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  • 9
    Electronic Resource
    Electronic Resource
    Normal ICOS, ICOSL and AID Alleles in Danish Patients with Common Variable Immunodeficiency (2005)
    Oxford, UK; Malden, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 61 (2005), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Common variable immunodeficiency, CVID, is a primary antibody deficiency characterized by decreased levels of serum immunoglobulin G (IgG), decreased IgA and/or IgM and recurrent infections. It is assumed to be heterogeneous group of disorders caused by different genetic defects. Some patients have decreased levels of class switched memory B cells and/or decreased levels of somatic hypermutation which points to defects in the germinal centre (GC) reactions as cause of the disease in these patients. The inducible costimulator, ICOS, and its' ligand, ICOSL, are both involved in and necessary for the GC reaction and so is activation-induced cytidine deaminase, AID. Therefore, we sequenced the ICOS, ICOSL and AID genes in a cohort of 34 Danish CVID patients. We found 13 new single nucleotide polymorphisms (SNP) in the intron regions of the ICOSL gene as well as one SNP in exon 3. However, none of these polymorphisms were associated with CVID. We did not find a previously reported CVID-causing ICOS gene deletion or any other unique mutations in the ICOS or AID genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.2005.001603.x
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  • 10
    Electronic Resource
    Electronic Resource
    Influence of Bacterial Endotoxins on Basophil Histamine Release Potentiation of Antigen- and Bacteria-Induced Histamine Release (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 41 (1986), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The histamine-releasing capability of lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but was found to enhance the histamine release caused by anti-IgE. Also the IgE-mediated histamine release caused by specific antigens (allergens or bacteria) in sensitized individuals was enhanced by LPS. The potentiating effect of LPS was observed in grass pollen and dog dander allergic patients as well as in patients sensitized to E. coli or Staph, aureus bacteria. No potentiation was obtained by exposure to unspecific allergens or bacteria to which the persons were not sensitized. Bacteria can release histamine by immunological or nonimmunological mechanisms, and only the immunological histamine release was found to be potentiated by LPS. It is speculated that endotoxins reinforce release of histamine caused by allergens in allergic patients or by bacteria in persons sensitized to these microorganisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1986.tb00288.x
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