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Biomedical subjects

S Norn

Publications and source records attributed to S Norn.

At least 91 records · Page 5Linked to original sources
PubMed1986

Bacteria and their products release histamine and potentiate mediator release: new aspects in airway diseases.

The possibility that bacteria and their products play a role in airway diseases, due to their capacity to release histamine, was investigated in blood leucocytes from patients suffering from respiratory diseases and from healthy individuals. The results clearly show that bacteria release histamine by immunological and non-immunological mechanisms and that endotoxins enhance mediator release caused by allergens in allergic patients or by bacteria in persons sensitized to these organisms. Furthermore, a great increase is obtained in mediator release by the combination of immunological and non-immunological mechanisms.

Adult↗
PubMed1985

Bacteria-induced histamine release. Examination of the bacterial cell wall components peptidoglycan, teichoic acid and protein A.

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.

Bacterial Physiological Phenomena↗
PubMed1985

Sensitive glass microfibre-based histamine analysis for allergy testing in washed blood cells. Results compared with conventional leukocyte histamine release assay.

The new microfibre method for allergy testing is based on basophil histamine release after challenge with suspected allergens in samples of 50 microliter washed blood cells. Released histamine is bound to microfibres and measured after removal of interfering substances by washing. The microfibre method was compared with the conventional leukocyte histamine release assay in 18 allergic patients tested with 10 different allergens. It was found that the same individuals responded with histamine release to the same allergens in both assays, and the number of responders was almost identical. Also the dose-response curves and the cell sensitivity were almost identical, which further substantiated identity between the results obtained by the new microfibre method and the conventional assay. A comparison between the microfibre method and in vivo provocation tests showed good agreement when comparing the number of positive and negative responses in these test. The new method overcomes the problems in allergy testing, where only small amounts of blood are available and many tests have to be carried out.

Allergens↗
PubMed1985

Inhibitory effect of cyclosporin A on histamine release from human leukocytes and rat mast cells.

The influence of cyclosporin A (CyA) on human basophil histamine release induced in vitro by specific antigen, anti-IgE, calcium ionophore A23187, or concanavalin A (Con A) was studied. CyA inhibited the release induced by these four stimulators. It is suggested that the drug acts directly on the target cell, since similar effect was obtained with isolated peritoneal rat mast cells. The basophil histamine release was not changed by a non-immunosuppressive cyclosporin derivate.

Animals↗
PubMed1984

A new method for detecting histamine release.

Glass microfibres have been found to bind histamine with high affinity and selectivity. A new test for measuring basophil histamine 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 microliter washed blood with 20 microliter antigen per well for 90 min at 37 degrees 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 fluorometric o-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.

Histamine↗
PubMed1984

Lectin-mediated reactions in histamine release caused by bacteria.

The bacteria-induced release of histamine was studied in human basophil leukocytes and in isolated rat mast cells. Whole bacteria of Staph. 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 of Staph. aureus interact with lectins on the basophil cell membrane leading to histamine release.

Adult↗
PubMed1984

Type I allergy to normal cellular constituents in chronic inflammatory bowel disease? Results from basophil histamine release test compared with total IgE and antinuclear antibodies.

The possibility of autoimmune type I reactions to cellular constituents was investigated in 22 patients with ulcerative colitis, 12 with Crohn's disease, and in 22 healthy volunteers. Nuclear components and colon mucosa fragments were tested as potential antigens by the basophil histamine release technique. One of 12 patients with ulcerative colitis responded to sonicated leukocyte nuclei and one of 12 patients with Crohn's disease responded to both nuclei and RNA. Increased serum levels of total IgE and antinuclear antibodies of IgE class were found in one and three of the 24 patients, respectively. Histamine release caused by colon mucosa fragments was not observed in a separate study consisting of 10 ulcerative colitis patients and 10 healthy volunteers. Autoimmune type I allergy to cellular constituents does not seem to be of significance for chronic inflammatory bowel disease and thus could not explain the involvement of tissue mast cells and eosinophils in this condition.

Adult↗
PubMed1984

Bacterial histamine release by immunological and non-immunological lectin-mediated reactions.

The mechanisms of bacteria-induced histamine release were examined in vitro in human leukocytes and rat mast cells. Three types of bacterial responders were found. In persons with IgE-bearing basophilocytes bacterial histamine release could be triggered by two different mechanisms, an IgE-dependent mechanism where removal of IgE abolished the release and a non-immunological mechanism where this was not the case. In responders with no IgE-bearing cells bacterial histamine release was caused by a non-immunological mechanism. The non-immunological mechanism was further substantiated by release in isolated mast cells from germ-free rats. These experiments suggest a direct interaction between bacteria and target cell, and experiments with multi-washed bacteria and bacteria cell wall preparations indicate the possibility of the bacteria wall interacting with the target cell. It is probable that the non-immunological mechanism depends on lectin-mediated reactions, since bacteria-induced histamine release was inhibited by lectin-binding sugars as is release caused by plant lectins.

Basophils↗
PubMed1984

Complexity of lectin-mediated reactions in bacteria-induced histamine release.

We have earlier suggested that bacteria-induced histamine release is caused by different mechanisms, including allergic and non-immunological mechanisms, and that the latter probably depends on lectin-mediated reactions. Two possibilities of lectin-mediated reactions were examined in this study, bacterial surface lectins bind to sugars on the basophil cell membrane leading to histamine release, and the reverse reaction where bacterial aminosugars react with lectins on the basophil cell surface. In the bacterial histamine release caused by the Staph. aureus strain Wood 46 it was possible to demonstrate a reverse reaction, but not a bacterial lectin-mediated reaction. The reaction seems to be complex, as lower concentrations of sugars might potentiate the release of histamine by binding to the target cell or bacteria, while the release is inhibited by higher concentrations.

Adult↗
PubMed1984

Allergic and pseudo-allergic reactions caused by penicillins, cocoa and peppermint additives in penicillin factory workers examined by basophil histamine release.

Allergic and pseudo-allergic reactions were examined in penicillin factory workers exposed to the dust of preparations of pivampicillin and pivmecillinam. Among 14 workers basophils from five persons showed histamine release by challenge with penicillins, whereas no release was observed in controls of non-atopic individuals not working with the manufacturing of penicillin. Positive skin response was obtained in four workers by path testing and in three persons by scratch test revealing late but no immediate response. All the eight workers who were also exposed to flavour additives used in the penicillin preparations showed histamine release by cocoa and peppermint. The release was not changed by removal of immunoglobulins from the basophil cell surface and the additives caused a similar release in the controls. The histamine release caused by cocoa and peppermint therefore depend on non-immunological mechanisms, i.e. pseudo-allergic reactions which might contribute to the symptoms in penicillin factory workers.

Allergens↗
PubMed1984

Staphylococcus aureus peptidoglycan induces histamine release from basophil human leukocytes in vitro.

Whole killed cells, cell walls, and peptidoglycans of Staphylococcus aureus were found to release histamine from human leukocytes and isolated rat mast cells in vitro. The histamine-releasing capability increased in the order of whole bacteria, cell walls, and peptidoglycans. Peptidoglycan was found to release histamine by a nonimmunological mechanism, as demonstrated by release in cells deprived of surface immunoglobulins, whereas whole bacteria and cell walls seemed to operate both by immunological and nonimmunological mechanisms. Histamine release was not a specific property of S. aureus; a wide range of whole bacterial species had this activity. We suggest that peptidoglycan may be a common factor responsible for histamine release by different bacteria.

Basophils↗
PubMed1984

Autoimmune type I reactions directed against nuclear components in rheumatoid arthritis.

Basophil histamine release was examined in leucocyte suspensions from patients with rheumatoid arthritis (RA) after challenge of the cells with isolated and sonicated leucocyte nuclei from normal individuals. Most of the patients with active disease responded with significant histamine release, whereas no response was obtained in the inactive patients and in normal controls. A similar pattern was found in the urinary excretion of the main metabolite of histamine, NT-methyl-imidazoleacetic acid, since an increased excretion was observed in most patients with severe disease activity in contrast to patients with moderate and quiescent activity and the control group. These findings strongly indicate an involvement of autoimmune allergic type I reactions in RA. The release of histamine and other mediators from basophils and mast cells may cooperate in the inflammatory reactions and the destruction of the joints in RA.

Adult↗
PubMed1983

Intrinsic asthma and bacterial histamine release via lectin effect.

Bacteria-induced histamine release from basophil leukocytes was observed in vitro in both children with intrinsic asthma (IA) as well as in normal individuals. In vivo the release is suggested to take place only in the lung of IA patients, where a defective pulmonary barrier would permit the bacteria to enter, but not in healthy individuals. The study indicates that two different mechanisms of bacterial histamine release might exist, an IgE-mediated reaction and a non-immunological mechanism consisting of a direct interaction with the basophil cell surface. The non-allergic mechanism might depend on a lectin effect where bacterial surface lectins interact with the basophil cell surface leading to release of histamine. Inhibition studies with carbohydrates suggest a multi-lectin reaction in the bacterial histamine release involving several types of lectins on the bacterial membrane reacting with different carbohydrate moieties on the cell surface of basophil leukocytes.

Asthma↗
PubMed1983

Inhibitory effect of calcium antagonists on histamine release from human leukocytes. In vivo and in vitro experiments.

A study was made of the influence of calcium antagonists on human basophil histamine release induced in vitro by specific antigen, anti-IgE or the calcium ionophore A23187. Both verapamil, nifedipine, and nimodipine were found to inhibit the release, and a similar effect was also observed after peroral administration of verapamil and nifedipine. The inhibitory effect of the drugs on histamine release seems to depend on interaction with calcium at different sites. The anti-allergic effect might explain the improvement found with calcium antagonists in exercise-induced asthma.

Antibodies, Anti-Idiotypic↗
PubMed1983

Basophil histamine release induced by leukocyte nuclei in patients with rheumatoid arthritis.

Leukocyte suspensions containing basophils were obtained from 23 patients with rheumatoid arthritis (RA). When these cells were incubated with leukocyte nuclei from normal persons, histamine release was seen in 11 of the 15 patients with active disease, but not in the quiescent group or in normal individuals. The dose-response curve for histamine release was similar to that obtained by specific antigen in type I allergy. By removal from and refixation to the cells of surface Ig, the release of histamine was respectively, abolished and restored, just as in similar experiments in hay fever patients. The dependence of pH for removal was also identical with that found in type I allergy. Antinuclear antibodies of the IgE class (IgE ANA) mainly directed against the granulocyte nuclei were often found in serum and on the cell surface of the RA patients, but not in normal individuals. A correlation was found between these titres in serum and on the cell surface. No correlation was found between ANA in serum and on the cell surface, on the one hand and disease activity and histamine release on the other. In a group of 12 patients with another joint disease, osteoarthrosis, only two patients showed histamine release, and in contrast to the other patients they showed swelling of more than two joints. The present investigation supports our hypothesis of an involvement of an autoimmune type I reaction directed against nuclear components in the RA disease.

Adult↗