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Biomedical subjects

S Norn

Publications and source records attributed to S Norn.

At least 73 records · Page 4Linked to original sources
PubMed1987

Effect of lysophosphatidylserine on immunological histamine release.

The effect of lysophosphatidylserine on immunological histamine release has been studied in rat peritoneal mast cells actively sensitized with horse serum and in human basophils challenged with anti-IgE. In contrast to other lysophospholipids, lysophosphatidylserine enhances the immunological histamine release in rat mast cells. The effect shows the kinetics of a saturable process with an apparent Km for lysophosphatidylserine of 0.26 microM. A similar Km value (0.21 microM) is found when measuring the non-immunological histamine release activated by lysophosphatidylserine plus nerve growth factor. A comparison with phosphatidylserine shows that a half-maximal response to lysophosphatidylserine occurs at a concentration 4-times lower. In addition, the magnitude of the response is higher. At variance with rat mast cells, lysophosphatidylserine does not influence the histamine release elicited by immunological and non-immunological stimuli in human basophils. The histamine secretion in these cells is instead affected by a calcium ionophore or tetradecanoylphorbolacetate, a compound producing activation of protein kinase C.

Animals↗
PubMed1987

Histamine release induced by bacteria. A new mechanism in asthma?

Bacteria release histamine from human basophil leukocytes and mast cells. The release can be caused by an immunological (IgE-dependent) mechanism, but mostly we found a non-immunological (lectin-mediated) mechanism which indicates that mediator release triggered by bacteria can occur without the person being sensitized to the micro-organism in question. Both bacteria and bacterial products such as endotoxins potentiate basophil histamine release caused by allergens in allergic patients or by bacteria in persons sensitized to the micro-organisms. It is therefore tempting to speculate that bacteria and their products might be of importance for asthma by their capacity to release histamine and to potentiate mediator release.

Asthma↗
PubMed1987

Complexity of the influence of gangliosides on histamine release from human basophils and rat mast cells.

The influence of exogenous addition of gangliosides on histamine release from human basophils and rat mast cells was examined in vitro. Gangliosides dose-dependently inhibited histamine release, and this inhibition was dependent on the ganglioside sialic acid content, since GT1b, having 3 sialic acid moieties, was more potent than gangliosides with 2 moieties (GD1a and GD1b), which again were more potent inhibitors than GM1 with one moiety. Asialo-GM1 was without effect. In high concentrations the gangliosides potentiated basophil histamine release. The modulation of histamine release was reflected in the sensitivity of the cells to extracellular calcium, since inhibition of the release could be counteracted by increasing the extracellular concentration of calcium.

Animals↗
PubMed1987

Membrane sialic acid influences basophil histamine release by interfering with calcium dependence.

The influence of the cell membrane content of sialic acid on basophil histamine release was examined in vitro in allergic patients and normal controls. Enzymatical removal of sialic acid enhanced histamine release induced by allergen and anti-IgE, whereas an increase in membrane sialic acid content by insertion of sialic acid containing gangliosides into the membrane inhibited the mediator release. The reduction in membrane sialic acid content abolished the inhibitory capacity of the calcium channel antagonist nimodipine, whereas the inhibition produced by verapamil and lanthanum was not affected. This difference, together with the previous finding that alterations in membrane sialic acid content is reflected in the cell sensitivity to extracellular calcium, suggest an interaction between membrane sialic acid and the calcium channels involved in basophil histamine release.

Basophils↗
PubMed1987

Bacteria and their products peptidoglycan and teichoic acid potentiate antigen-induced histamine release in allergic patients.

Histamine release was examined in leukocyte suspensions from patients allergic to grass pollen, mite or cat dander or to bacteria (antigen). When the cells were challenged with specific antigen plus bacteria to which the person was not sensitized, these bacteria were found to potentiate the allergic histamine release. The potentiating effect by bacteria might be due to the bacterial cell wall components, peptidoglycan and teichoic acid, which mimic the effect of bacteria.

Antigens, Bacterial↗
PubMed1987

Impaired basophil histamine release from allergic patients.

A few patients (6-7%) with a verified type I allergic reaction do not respond with histamine release after challenge of their basophils with specific antigen (non-responding basophils from allergic patients). Sera from these non-responding patients were used for passive sensitization of responding cells from healthy controls. When these sensitized cells were challenged with specific antigen, histamine release was observed indicating that the non-responding allergic patients have circulating antigen-specific IgE capable of binding to Fc-receptors on the basophils. These findings suggest the possibility that non-responding basophils have impaired cell functions. We therefore examined the influence of enhanced IgE receptor stimulation on histamine release in non-responding basophils. This was made by stimulating protein kinase C activity by a phorbol ester (phorbol 12-myristate 13-acetate). When the non-responding cells were incubated with the phorbol ester and challenged with either anti-IgE or specific antigen, the cells released histamine. These findings support the hypothesis that the unresponsiveness of basophils in some allergic patients is associated with impaired IgE receptor complex activation or subcellular functioning and not with a lack of cell-bound IgE.

Asthma↗
PubMed1987

Non-IgE-dependent bacteria-induced histamine release from human lung and tonsillar mast cells.

A wide spectrum of formalin-killed bacteria have been tested for their ability to release histamine from human dispersed lung and tonsillar mast cells. Escherichia coli, Enterobacter cloacae, Staphylococcus epidermidis, Proteus vulgaris, Klebsiella oxytoca and K. pneumoniae were the most effective histamine releasers. Further studies on tonsillar mast cells showed that E. coli-induced histamine release differed from IgE-dependent release with respect to its kinetics, temperature and pH profiles and its sensitivity to calcium deprivation and metabolic inhibitors. A lectin-mediated mechanism may operate, but other non-immunological mechanisms might also be involved in the release. Escherichia coli and anti-IgE did not synergize in inducing histamine release. The production of PGD2 and the failure to detect lactate dehydrogenase following incubation of mast cells with E. coli suggests that histamine release is not due to cytotoxicity.

Adult↗
PubMed1987

Comparison of the action of calcium antagonists on basophil histamine release.

The inhibitory capacity of calcium antagonists on basophil histamine release was examined in allergic patients and in controls. All dihydropyridines tested (nifedipine, nimodipine, nitrendipine, nicardipine, felodipine) dose-dependently inhibited anti-IgE- and A23187-induced release with an order of potency of felodipine greater than nicardipine greater than nifedipine = nimodipine = nitrendipine. Only the inhibition induced by felodipine and nicardipine on anti-IgE-induced release could be counteracted by increasing extracellular calcium. Diltiazem, not belonging to the dihydropyridines, was a weak inhibitor. A combination of felodipine and verapamil in low concentrations exerted a synergistic inhibitory effect on histamine release, whereas this was not the case with other combinations of antagonists. The results suggest differences in the mode of action of the 1.4-dihydropyridines. This might be of significance in the search for calcium antagonists suitable in the treatment of allergic diseases.

Antibodies, Anti-Idiotypic↗
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

Histamine release from basophil leukocytes induced by microbial antigen preparations in patients with AIDS.

Type I allergy against some common microorganisms was investigated in 14 patients with AIDS and 11 human immunodeficiency virus (HIV) antibody-positive homosexual men, and in a control group consisting of 13 heterosexual men without HIV antibodies. Basophil histamine release technique was used as a sensitive method to detect type I allergy against Candida albicans (CA), Herpes simplex virus type I (HSV-I) and cytomegalovirus (CMV). Of the 14 AIDS patients 11 (78%) showed significant histamine release when stimulated with CA, and HSV-I caused release in 10 (71%), whereas no response was obtained by CMV. In the group of HIV antibody-positive men only one released histamine when stimulated with CA and HSV-I and this patient also had lymphadenopathia. In contrast to these results, no release of histamine was obtained in the control group consisting of 13 heterosexual men. The histamine release caused by CA and HSV-I is mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell-bound immunoglobulins. These results suggest an involvement of type I allergy as a pathogenetic co-factor in some infections in AIDS, and allergic type I reactions to CA and HSV-I might be an indicator for the presence of manifest AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Influence of nimodipine, verapamil and lanthanum on histamine release from human basophils: effect of pretreatment with sialidase.

Our previous studies suggest that the membrane content of sialic acid influences histamine release from human basophils by interfering with the transmembraneous calcium fluxes preceding histamine release. In this study we investigated a possible interaction between membrane sialic acid and the calcium channels, using the calcium antagonists nimodipine, verapamil and lanthanum. Anti-IgE-induced histamine release was inhibited by verapamil, nimodipine and lanthanum. When cells were pretreated with sialidase in order to remove sialic acid from the cell membrane, the inhibitory action of nimodipine was abolished, whereas the inhibition by verapamil or lanthanum was unaffected. This difference may be explained by the different mode of action of the calcium channel antagonists, and the results suggest an association between membrane sialic acid and the calcium channel.

Basophils↗
PubMed1986

Enhancement of histamine release from human basophils pretreated with different sialidases.

Histamine release from human basophils was investigated in vitro after removal of cell membrane sialic acid by three different sialidases. Pretreatment of the cells with sialidases from Cl. Perfringens, V. Cholera or Influenza virus A2 enhanced histamine release induced by subsequent stimulation of the cells with anti-IgE or the plant lectin Concanavalin A and caused a shift to the left of the dose-response curve for anti-IgE. The enhanced histamine release was reflected in a increased calcium sensitivity, thus suggesting that cell membrane sialic acid might be involved in the calcium fluxes preceeding histamine release. In higher doses the sialidase from Cl. Perfringens caused the cells to release histamine by itself, whereas the sialidases from V. Cholera and Influenza virus A2 in high doses inhibited the cell response to Concanavalin A.

Basophils↗
PubMed1986

Endotoxins release histamine by complement activation and potentiate bacteria-induced histamine release.

The histamine-releasing capability of bacterial lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but it was found to enhance the histamine release caused by bacteria in basophils from persons sensitized to these bacteria. In the presence of serum, LPS was able to release histamine through complement activation. It is speculated that endotoxins reinforce release of histamine caused by bacteria in persons sensitized to these microorganisms, and a direct mediator release via complement activation might play a role in septic conditions.

Bacteria↗
PubMed1986

Influence of bacterial endotoxins on basophil histamine release. Potentiation of antigen- and bacteria-induced histamine release.

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.

Allergens↗
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↗