Carsten Strøby Jensen

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.

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.

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.

The survival of the Danish model : a historical sociological analysis of the Danish system of collective bargaining

Part 1 A theoretical basis for the analysis of industrial relations - the development of institutions: the end of institutions? Part 2 The Danish system of collective bargaining - the origins of the Danish system negotiation rules and concatenation the third actor structural stagnation. Part 3 Centralized decentralization - complementary concepts: degrees of centralization a surge in structural development towards the year 2000.

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.

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 (lectinmediated) 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.

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.

Neofunctionalist Theories and the Development of European Social and LabourMarket Policy

This article discusses whether traditional neofunctionalist theories are relevant in the analysis of political integration in Europe. The discussion is based on an analysis of the development of co‐operation on social and labour market issues in the EU since the mid‐1980s. The role of supranational actors, particularly the Commission, is examined in connection with the development of co‐operation on social and labour market issues. It concludes that the neofunctionalist concept of ‘spillover’ is useful in the attempt to explain political integration in the social policy and labour market fields. The article makes a case for the revision of traditional neofunctionalist theories so as to incorporate concepts that capture the increasingly significant impact of treaty revisions in connection with the development of co‐operation in these fields. The concept of institutional/legalistic spillover is introduced to illustrate the integrative effects of the treaty negotiations on the development of co‐operation.

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.

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 A231B7, 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 by the cell to extracellular calcium, NANA in the cell membrane glucocalyx thus seems to modulate the basophil response to stimulation by modulating transmembrancous calcium transport.