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  • 1
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this study of intrinsic asthma (IA) in children the pathogenic role of bacteria in respiratory disease was elucidated by a basophil histamine liberation technique. Several strains of bacteria caused release of histamine from peripheral leukocytesin vitro. Normal, non-infectious and non-atopic children frequently responded in a similar fashion, although positive responses were less frequent. It seems that two different mechanisms of bacterial histamine release exist: interaction with the basophil-bound IgE and a direct interaction with the cell surface. It is suggested that the histamine release takes place only in the lung of IA patients, where a defective pulmonary barrier could permit the bacteria to enter, but not in healthy individuals.
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The bacteria-induced release of histamine was studied in human basophil leukocytes and in isolated rat mast cells. Whole bacteria ofStaph. aureus caused release in a 98% pure population of peritoneal mast cells from germ-free rats, indicating a non-immunological mechanism and a direct interaction between the bacteria and the target cells. Probably the bacterial cell wall interacts with the cell membrane, since a preparation of the bacterial cell wall caused a dose-dependent release of histamine from basophil leukocytes similar to that induced by whole bacteria, and repeated washing of whole bacteria did not change the release. Inhibition studies by lectin-binding sugars indicate that aminosugars on the bacterial surface ofStaph. aureus interact with lectins on the basophil cell membrane leading to histamine release.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 14 (1984), S. 414-416 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Glass microfibres have been found to bind histamine with high affinity and selectivity. A new test for measuring basophil hisamine release has been developed using the glass microfibres as a solid phase. Glass microfibres are crushed and fixed to the bottom of microtitre plates with a water-soluble glue. Histamine release is performed in the glass microfibre-prepared microtitre plates by challenging 100 μl washed blood with 20 μl antigen per well for 90 min at 37°C. Released histamine is bound with high affinity to the glass microfibres, since 90% of histamine in the solution is adsorbed to the fibres. After incubation the microtitre plate is washed with H2O to remove cells and interfering substances. Fibre-bound histamine is detected by the fluorometrico-phthaldialdehyde method. The sensitivity of the assay is 0.63 ng histamine, 2 HCl and the histamine standard curve is linear up to at least 5 ng histamine, 2 HCl. Optimal conditions for the new assay are described. After challenge with anti-Ige a comparison with the conventional histamine release from Ficoll-Hypaque-isolated leukocytes showed almost identical results.
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The histamine-releasing capability of whole bacteria was examined in leukocyte suspensions from normal individuals. Both gram-positive and gram-negative bacteria caused basophil histamine release. It is probably the bacterial cell wall which interacts with the basophil cell surface leading to release of histamine, since cell walls showed higher histamine releasing capability than the whole bacteria. The releasing effect of the bacterial cell wall components peptidoglycan, teichoic acid and protein A was examined. The peptidoglycan preparations were found to be more potent than the corresponding whole bacteria and cell walls. Since peptidoglycan is found in the cell wall of both gram-positive and gram-negative bacteria, it might be a common factor responsible for histamine release by different bacteria. No release was obtained by teichoic acid, whereas protein A caused histamine release in leukocytes from allergic patients, but only a poor release in normal individuals. The initial step in protein A-induced histamine release might be a binding of protein A to IgE on the cell surface, since removal of cell-bound IgE reduced the release and a high correlation was found between protein A- and anti-IgE-induced histamine release.
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  • 5
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine release from human basophil leukocytes was triggered byStaph. aureus or by complement activation caused by endotoxins isolated fromE. coli or Salmonella bacteria. Influenza A virus was found to enhance the mediator release and the effects was caused by synergism, since the virus itself did not release histamine. The potentiating effect of the virus was abolished by a potent neuraminidase inhibitor. Furthermore, a purified neuraminidase preparation obtained fromVibrio cholerae caused a similar potentiating effect, which was also abolished by the neuraminidase inhibitor. These findings indicate that the neuraminidase on the surface of influenza A virus is responsible for the potentiating effect of the virus on basophil histamine release.
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  • 6
    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.
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  • 7
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine release caused by anti-IgE was examined in leukocyte suspensions from 10 healthy individuals. Influenza A virus was found to enhance the histamine release but did not release histamineper se. When monoclonal antibodies directed against the viral neuraminidase were included in the samples, the potentiating effect of the virus was completely abolished. The same occurred using a neuraminidase inhibitor. However, monoclonal antibodies directed against the viral haemagglutinin also abolished the potentiation. A binding of virus to the basophil cell surface by haemagglutinin therefore seems to be necessary for the viral neuraminidase to cause potentiation of mediator release.
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  • 8
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine release from human basophil leukocytes was triggered byStaph. aureus, Salmonella enteriditis, non-haemolytic streptococci, orE. coli. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus did not induce release of histamineper se. This potentiating effect of the virus was seen both when the bacteria-induced histamine release was IgE-dependent (i.e. patient sensitized to the bacterium) and when the bacterium caused mediator release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Histamine release induced by anti-IgE and calcium ionophore or agarose-beads was also enhanced in the presence of the virus. These findings indicate that influenza A virus potentiates both IgE-and non-IgE-mediated histamine release induced by bacteria and other stimulators.
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  • 9
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Experimentsin vitro have shown that bacteria induce histamine release and potentiate IgE-mediated histamine release. In the present study, these events were examined in allergic patients by anin vivo model using nasal challenge. Nasal spray with 56 mgStaphylococcus aureus triggered histamine release in the nasal cavity in 4 of 13 patients, whereas no response was obtained by 28 and 112 mg bacterium. These findings indicate that bacteria containing peptidoglycan may release histaminein vivo. To avoid allergens, we used anti-IgE antiserum. In six patients nasal challenge with anti-IgE (112000 IU) caused an, increased histamine level in the nasal fluid which was not obtained by a control preparation without anti-IgE antibodies. The IgE-mediated mediator release was potentiated by the bacterium in only 2 of 22 patients.
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  • 10
    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.
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