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Biomedical subjects

P Clementsen

Publications and source records attributed to P Clementsen.

51 records · Page 3Linked to original sources
PubMed1989

Influenza A virus enhances allergic histamine release. Effect of neuraminidase.

Histamine release was examined in leukocyte suspensions from patients allergic to house dust mite, grass pollen, birch pollen or cat dander. Influenza A virus was found to enhance the antigen-induced mediator release, but did not cause release of histamine from the cells per se. Also histamine release induced by anti-IgE in cell suspensions from normal individuals was enhanced by virus. The potentiating effect of influenza A virus might be due to neuraminidase on the surface of virus, since a similar effect was caused by a purified neuraminidase obtained from Vibrio cholerae, and the effect of virus as well as the neuraminidase was completely abolished by a potent neuraminidase inhibitor. The synergistic enhancement in IgE-mediated histamine release by virus could be of significance for the conversion from latent to manifest asthma.

Adult↗
PubMed1989

Influenza A virus enhances Staphylococcus aureus-induced basophil histamine release in normal individuals and patients with intrinsic asthma.

Influenza A virus was found to enhance Staphylococcus aureus-induced histamine release in human leukocyte suspensions, but did not per se release histamine. This potentiating effect was found to be similar in cells from normal individuals and from patients with intrinsic asthma. The enhancement of mediator release could be due to viral neuraminidase on the surface of the virus, since a similar potentiating effect was caused by a purified neuraminidase preparation obtained from Vibrio cholerae, and the effect of virus as well as of the purified neuraminidase was completely abolished by a potent neuraminidase inhibitor. The potentiating effect of virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections.

Adult↗
PubMed1988

Virus enhances histamine release from human basophils.

Histamine release from human basophil leukocytes was triggered by Staph. aureus or by complement activation caused by endotoxins isolated from E. coli or Salmonella bacteria. Influenza A virus was found to enhance the mediator release and the effect 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 from Vibrio 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.

Basophils↗
PubMed1988

Influenza A virus potentiates basophil histamine release caused by endotoxin-induced complement activation. Examination of normal individuals and patients with intrinsic asthma.

Histamine release from human basophil leukocytes was triggered by complement activation by means of endotoxins isolated from E. coli and Salmonella bacteria. Influenza A virus was found to enhance the mediator release, and the effect was caused by synergism, since virus itself did not release histamine. The potentiating effect was similar in cells from normal individuals and from patients with intrinsic asthma. The involvement of viral neuraminidase was examined by a potent neuraminidase inhibitor and this inhibitor completely abolished the potentiating effect by virus. A purified neuraminidase preparation obtained from Vibrio cholerae caused a similar potentiating effect in mediator release and the effect was abolished by the neuraminidase inhibitor. These findings indicate that viral neuraminidase is responsible for the potentiating effect of virus on the histamine release. This effect might play a role in septic conditions and possibly contribute to asthmatic attacks by infections.

Aged↗
PubMed1988

Bronchial asthma: pathophysiological mechanisms and corticosteroids.

The clinical effects in asthma of corticosteroids can be ascribed to their strong anti-inflammatory action. The pathophysiology of asthma is complex. A diversity of mediators and interactions between mediators and between mediators and various cell types enhances and maintains the inflammatory process in the airways resulting in severe asthma. This is a vicious circle. Penetration through the airway epithelium of allergens and other insulting particles trigger release of inflammatory mediators and neurotransmitters, which, by chemotaxis and activation of inflammatory cells, results in enhanced and prolonged mediator release. Several of these mediators possess tissue-toxic properties enhancing the airway inflammation. The glucocorticoids have several points of action affecting both mediator release and accumulation and activation of inflammatory cells, which explains their favourable effect in asthma.

Adrenal Cortex Hormones↗
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

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

Syncope due to right atrial thromboembolism: diagnostic importance of two-dimensional echocardiography.

Recurrent syncopes due to acute circulatory failure occurred in a 40-years-old female with a massive right atrial thromboembolus which was detected by two-dimensional echocardiography (2 DE), and subsequently surgically removed. 2 DE is an excellent and rapid screening technique for the patients with right sided intracardiac masses. The use of 2 DE should be considered for patients with unclear syncopes e.g. postoperatively, following deep venous thrombosis or in cases resembling "hyperventilation syndrome".

Adult↗