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Biomedical subjects

S Norn

Publications and source records attributed to S Norn.

At least 55 records · Page 3Linked to original sources
PubMed1990

Virus enhances IgE- and non-IgE-dependent histamine release induced by bacteria and other stimulators.

Histamine release from human basophil leukocytes was triggered by Staph. aureus, Salmonella enteritidis, non-haemolytic streptococci, or E. 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 histamine per 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.

Bacterial Infections↗
PubMed1990

Cytokine-induced release of histamine from basophil leukocytes from AIDS patients.

Cytokine-induced histamine release from basophil leukocytes was examined in cell suspension from AIDS patients and compared with healthy controls. Cells from approximately half of the AIDS patients, in contrast to none from the control group, showed histamine release after stimulation with interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), lymphotoxin (LT) and interferon gamma (IFN gamma). These cytokines seem to induce histamine release from cells from AIDS patients by interaction with the cell surface immunoglobulins, since removal of the immunoglobulins prior to the exposure of the cytokines completely abolished the response to the cytokines. IL-1 alpha, IL-1 beta, IL-3, colony stimulating factor (CSF) and granulocyte-macrophage-CSF (GM-CSF) caused significant histamine release from cells from a similar number of AIDS patients and controls.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Endotoxin from Haemophilus influenzae enhances IgE-mediated and non-immunological histamine release.

Haemophilus influenza and its extracellular products (EP) did not release histamine from basophil leukocytes in cell suspensions from normal individuals, patients with chronic bronchitis or patients allergic to either house dust mite, grass pollen, cat dander or to their own bacteria. However, the EP was found to enhance their basophil histamine release. IgE-mediated histamine release was examined by stimulation of the cells with anti-IgE or the specific allergens, and non-immunological histamine release by stimulating the cells with the calcium ionophore A23187 or Staphylococcus aureus. In all the experiments EP caused a significant increase in the histamine release. When H. influenzae endotoxins were removed from the EP, the potentiating effect of EP was completely abolished, whereas heating (80 degrees C, 30 min) or treatment of EP with proteinase did not influence the potentiating effect. These results indicate that H. influenzae endotoxin potentiates histamine release caused by IgE-mediated reactions or by non-immunological mechanisms.

Adult↗
PubMed1990

Bacteria and endotoxin enhance basophil histamine release and potentiation is abolished by carbohydrates.

Histamine release caused by anti-IgE, specific antigens and calcium ionophore A23187 was examined in leukocyte suspensions from healthy individuals and patients allergic to house dust mite and birch pollen. Staphylococcus aureus and LPS from Salmonella typhimurium were found to cause a synergistic enhancement of the release. The potentiation of mediator release by the bacteria and the endotoxin depends on a binding to the basophilocyte, followed by a non-transient event, since the potentiating effect persists after preincubation of the cells with the LPS followed by washout and leaving the cells for 30 min at 37 degrees C before stimulation with anti-IgE. The potentiation was abolished or reduced by galactose (10(-7) and 10(-6) M) and N-acetylglucosamine (10(-6) and 10(-5) M), acting by a binding to the basophil cell membrane, demonstrated by the persistence of effect after preincubation and washout of unbound sugar.

Adult↗
PubMed1990

Influenza A virus potentiates bacteria-induced histamine release. Examination of normal individuals and patients allergic to bacteria.

Influenza A virus was found to enhance basophil histamine release induced by Escherichia coli, Salmonella enteritidis, Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus sanguis, but did not per se release histamine. This potentiating effect of the virus was seen both when the bacteria-induced mediator release was IgE-dependent (i.e. patient allergic to bacterium) and when the bacterium caused histamine release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Also histamine release induced by other immunological and non-immunological stimuli, such as anti-IgE, calcium ionophore or agarose beads was enhanced in the presence of the virus. The potentiating effect of the virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections.

Adult↗
PubMed1990

Influenza A virus enhances basophil histamine release and the enhancement is abolished by carbohydrates.

Basophil histamine release was studied in leukocyte suspensions from normal individuals and from patients allergic to house dust mite or birch pollen. Mediator release caused by IgE-mediated reactions was examined by stimulating the cells with anti-IgE or specific antigens, and the calcium ionophore A23187 was used for a non-immunological histamine release. In all experiments influenza A virus caused a synergic enhancement of the mediator release and the potentiation was abolished by galactose (10(-7) to 10(-6) M) and by 10(-6) to 10(-5) M of N-acetylglucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. Wash-out experiments show that the sugars prevent the aggravation of mediator release by a binding of sugar to the basophil cell membrane, thereby causing a blockade of binding sites responsible for the potentiating effect of virus.

Adult↗
PubMed1989

HIV antigen stimulates basophil leukocytes from AIDS patients to release histamine due to type I allergy.

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.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Influenza A virus enhances IgE-mediated histamine release from human basophil leukocytes. Examination of the effect of viral neuraminidase and haemagglutinin.

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 histamine per 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.

Antibodies, Anti-Idiotypic↗
PubMed1989

Staphylococcus aureus and influenza A virus stimulate human bronchoalveolar cells to release histamine and leukotrienes.

Mediator release was examined from superficially lying cells in the airway epithelium obtained by bronchoalveolar lavage (BAL) in 13 non-atopic individuals. The BAL-cells were incubated (20 min, 37 degrees C) with Staphylococcus (Staph.) aureus or with human influenza A virus Staph. aureus was found to release histamine from cells from 7 of the 13 individuals and influenza A virus in 3 of 5 persons. Furthermore, Staph, aureus stimulated the BAL-cells to release leukotriene B4 in 7 of 11 subjects, whereas no release was found by influenza A virus in 7 examined persons. When cells from 4 persons were stimulated with Staph. aureus no release of leukotriene C4 was found. The mediator release caused by bacteria and virus might be of importance for the exacerbation of bronchial asthma in upper respiratory tract infections, since histamine is assumed to increase the epithelial permeability with entrance of allergens and other insulting particles, and leukotriene B4 facilitates airway inflammation.

Adult↗
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↗
PubMed1989

Determination of immunoglobulins responsible for histamine release induced by microbial antigens in AIDS patients.

AIDS patients in contrast to healthy individuals show basophil histamine release by stimulation in vitro of their blood leukocytes with Candida albicans (CA) and Herpes simplex virus Type I (HSV-I). Passive sensitization of cells from healthy individuals with the patient serum or surface immunoglobulins (Ig) derived from leukocytes of AIDS patients caused histamine release by the following stimulation of the cells with CA or HSV-I. When IgE was removed from the surface Ig no response was obtained, whereas a removal of IgG did not diminish the response. In contrast, no passive sensitization was obtained by serum derived from healthy individuals. The results show that IgE is responsible for the histamine release caused by CA and HSV-I in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Type I reactions directed against Pneumocystis carinii in AIDS patients.

Type I allergy directed against Pneumocystis carinii (PC) has been investigated in 14 patients with AIDS. The Pneumocystis carinii pneumonia often shows a rapid and severe course, and type I allergy against the parasite might be a pathogenic co-factor in the interstitial lung inflammation. In twelve of the AIDS patients the clinical symptoms and course of illness indicated a PC pneumonia. The basophil histamine release test was used as a sensitive test to detect type I allergy against PC. Eight of the patients showed significant histamine release when stimulated with PC. In contrast, only two patients in the group of 12 HIV antibody-positive homosexual men and none in the control group of 13 heterosexual men released histamine. The histamine release was 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 before the antigen challenge. The results suggest an involvement of type I allergy as a pathogenic co-factor in Pneumocystis carinii pneumonia.

Acquired Immunodeficiency Syndrome↗
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↗
PubMed1988

Basophil histamine release in children with adverse reactions to cow milk. Comparison with RAST and skin prick test.

Basophil histamine release was examined in 26 children suspected of having cow milk allergy (CMA). Following oral challenge with cow milk, the initial adverse reaction reappeared in 20 children, the majority developing urticaria. The urticaria patients showed a high degree of correlation between the results of histamine test, RAST and skin test. Children with gastrointestinal symptoms reacted to milk challenge, but only a few showed a positive histamine test, RAST and skin test. Among the patients with atopic dermatitis, the tests gave mostly negative results, which was in accordance with the lack of response to a milk challenge. The results obtained by removal from and fixation to the cell surface of IgE indicate an IgE-mediated reaction in CMA, which, in connection with the correlation between histamine test and RAST or skin test, suggests basophil histamine release as a suitable method for testing Type I allergy in children suspected of CMA.

Animals↗