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Biomedical subjects

S Norn

Publications and source records attributed to S Norn.

At least 37 records · Page 2Linked to original sources
PubMed1994

Microorganism-induced or enhanced mediator release: a possible mechanism in organic dust related diseases.

Bacteria were found to trigger mediator release, including histamine, leukotriene B4, and prostaglandin D2. Furthermore, histamine release caused by allergens as well as by nonimmunological reactions was enhanced by bacteria, endotoxins, and spores from molds. Mediator release and its enhancement play a crucial role for bronchoconstriction and inflammatory events in the airways. These effects of allergens, microorganisms, and other noxious agents in dusts may, therefore, in concert be responsible for the symptoms in organic dust related diseases.

Air Microbiology↗
PubMed1994

Bacteria-induced IgE-mediated histamine release: examination of patients with chronic bronchitis (CB) during acute exacerbations.

Twelve patients hospitalized with acute exacerbations of chronic bronchitis (CB) and infected in the lower respiratory tract with H. influenzae (HI) or Streptococcus pneumoniae (SP) were examined. Bacteria, isolated from the expectorate caused an IgE-mediated histamine release from the patient's own blood leukocytes, indicating that all were sensitized to their own bacteria. Sensitization was only observed in some of the patients when tested with a standard panel of HI or SP obtained from other patients, indicating the importance of using the patient relevant bacterial antigenic determinants. No sensitization was found in twelve controls. The patients showed cellular hyperreactivity to HI and SP, i.e. the releasability was higher than in the control group. The cellular hyperreactivity was not dependent on sensitization since it was also found against the non-infecting species. Both sensitization and cellular hyperreactivity may contribute to the aggravation of the disease.

Aged↗
PubMed1994

Increased numbers of circulating basophils with decreased releasability after administration of rhG-CSF to allergic patients.

Preliminary studies in hematological patients have indicated that treatment with rhG-CSF reduces basophil releasability ex vivo. We examined this phenomenon further, in allergic patients. Ten patients with grass pollen rhinoconjunctivitis were given rhG-CSF (5 micrograms/kg/day s.c.) for 5 days, and examined before and after treatment. Basophil counts increased from 5 to 19 x 10(9)/l (P < 0.01). Total blood histamine increased from 80 to 160 micrograms/l (P < 0.01), corresponding to a decrease in average basophil histamine content from 1.5 to 0.81 pg/cell (P < 0.01). Isolated mononuclear cells showed a significantly decreased histamine release (HR) when stimulated with A23187 and grass. Whole blood experiments showed a similar decreased HR to grass and anti-IgE (P < 0.01). However, we found an increase in total blood histamine. We conclude that treatment with rhG-CSF (1) increases the number of circulating blood basophils, (2) reduces the average histamine content per basophil, and (3) reduces the basophil releasability. These findings could be due to the mobilization of immature basophils from the bone marrow.

Adult↗
PubMed1993

Histamine-releasing serum factors as a predictor of the outcome of insect sting reactions. Results from a multicentre study.

Cord blood cells were incubated (passively sensitized) with sera from 27 patients with previous systemic reactions to insect stings. Histamine release (HR) from these cells was measured following exposure to venom extracts at increasing concentrations. The aim was to see whether this parameter could predict more efficiently than RAST and skin test the outcome of a subsequent re-sting. Results showed that HR from passively sensitized cells tended to reflect skin sensitivity and specific IgE levels. If patients were not re-stung during the follow-up period, HR from the passively sensitized cells frequently decreased whereas an increase was seen (in 6/13) when using sera collected after re-sting. In conclusion HR from passively sensitized cord blood cells could not satisfactorily predict re-sting reactions in the serum donors.

Fetal Blood↗
PubMed1991

[Respiratory tract infection and acute deterioration of obstructive lung disease].

Respiratory infection may aggravate chronic obstructive pulmonary disease. Viral respiratory infections may aggravate asthma, particularly in young individuals. Respiratory Syncytial virus and Rhinovirus dominate in children while, in adults, Influenza or Rhinovirus infections are most frequently concerned. Viral respiratory infections may also cause exacerbation of chronic bronchitis. Bacteria and their products scarcely play any part in asthmatic disease but may possibly aggravate chronic bronchitis and other forms of obstructive respiratory disease. In particular, Haemophilus influenzae and Streptococcus pneumoniae and bacterial endotoxin appear to be of significance. The mechanisms of the effects of viruses have several points of attack: Destruction of epithelium, release of mediators, potentiation of mediator-release and reduced beta-adrenergic function. Bacteria and their products may, similarly, cause bronchoconstriction and may, in vitro, release mediators and potentiate release of mediators.

Bacterial Infections↗
PubMed1991

Bacteria-induced histamine release from human bronchoalveolar cells and blood leukocytes.

Histamine release induced by Staphylococcus aureus was examined in cells obtained by bronchoalveolar lavage (BAL) in non-atopic individuals. Approximately half of the individuals responded with mediator release to the bacterium, and the release was found to be time- and concentration dependent. No difference was found between the patients who responded and those who did not respond in regard to age, sex, smoker/non-smoker, % recovery of BAL-fluid, total cell count, differential cell counts, histamine content per mast cell, or diagnoses. Also stimulation of the BAL-cells with the calcium-ionophore A23187 resulted in histamine release. S. aureus-induced histamine release from basophils was examined in leukocyte suspensions obtained from the same individuals, and in all experiments release was found. The dose-response curves were similar to those obtained with BAL cells. The bacteria-induced mediator release from superficially lying cells in the airways epithelium might be of importance for the precipitation or exacerbation of bronchial asthma in respiratory tract infections.

Adult↗
PubMed1991

Cytokine-induced histamine release from basophils of AIDS patients. Interaction between cytokines and specific IgE antibodies.

Basophil leukocytes obtained from AIDS patients, allergic patients and healthy controls were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8-17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig-dependent mechanism. Passive sensitization with cell-derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell-bound IgE was responsible for the cytokine-induced histamine release in AIDS patients. This response may be mediated by cytokine-selective IgE antibodies.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Virus, bacteria and lipopolysaccharide increase basophil cell response to histamine releasing stimulators and calcium. Examination of allergic and normal individuals.

Histamine release from human basophil leukocytes from allergic patients or controls was induced by specific antigens, anti-IgE or calcium ionophore A23187. Influenza A virus, S. aureus and lipopolysaccharide from S. typhimurium increased the maximum release of histamine and caused a shift to the left of the dose-response curves showing increased cell sensitivity and lowering of the threshold to these stimuli. The mechanism of action was elucidated by examining the mediator release as a function of increasing extracellular concentration of calcium. In these experiments the dose-response curves were changed by the microorganisms and lipopolysaccharide as before. This indicates that the microorganisms and lipopolysaccharide change the basophil cell response to IgE-dependent and non-immunological stimuli by causing a change in the subcellular handling of calcium.

Adult↗
PubMed1990

Carbohydrates inhibit the potentiating effect of bacteria, endotoxin and virus on basophil histamine release.

Histamine release caused by calcium ionophore A23187 and anti-IgE was examined in leukocyte suspensions from 8 healthy individuals. Staphylococcus aureus, lipopolysaccharide (LPS) from Salmonella typhimurium and influenza A virus were found to enhance the histamine release but did not release histamine per se. The potentiation of mediator release depends on a non-transient signal since the potentiating effect was also obtained by preincubation of the cells with LPS followed by wash-out and stimulation of the cells with anti-IgE. The potentiation was abolished or reduced by galactose, N-acetyl-glucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. These findings indicate that the enhancement of mediator release by bacteria, endotoxin, and virus depends on a sugar-mediated reaction.

Basophils↗
PubMed1990

Haemophilus influenzae potentiates basophil histamine release possibly by its endotoxins.

Haemophilus influenzae and its extracellular products (EP) did not release histamine in leukocyte suspensions from normal individuals. However, the EP were found to enhance basophil histamine release triggered by anti-IgE and by the calcium ionophore A23187. Experiments with EP indicate that it is the content of endotoxins which is responsible for the potentiating effect. Removal of endotoxin from the EP thus completely abolished the potentiating effect, whereas inactivation of its protease and proteins by heat-treatment or by proteinase K did not change the potentiation. A reinforcement of mediator release by the extracellular products of H. influenzae might play a pathophysiological role in chronic obstructive pulmonary disease.

Basophils↗