interleukin-8 and Bronchial-Spasm

Exercise-induced asthma is considered in terms of the stimulus, the intermediary pathway and the response. Various controversies about each of these components are discussed. The stimulus may be cooling of the airways, loss of water or neither of these, and there is evidence for and against the identity of exercise- and hyperventilation-induced asthma. The intermediary pathway seems certain to involve the release of chemical mediators, although other neurogenic mechanisms have been proposed. Since the response is far from uniform, it may well be that different pathways are involved in different subjects. The effector mechanism appears to be bronchospasm, but recent evidence has suggested that an inflammatory response may be involved in a late reaction to exercise. The variability of exercise-induced asthma may well be due to variations in intrinsic bronchial reactivity resulting from allergenic stimulation.

Topics: Asthma; Asthma, Exercise-Induced; Bicycling; Body Temperature Regulation; Bronchial Spasm; Chemotactic Factors; Humans; Humidity; Interleukin-8; Reflex, Abnormal; Respiration; Running; Swimming; Vagus Nerve

Topics: Animals; Asthma; Bronchial Provocation Tests; Bronchial Spasm; Chemotactic Factors; Humans; Inflammation; Interleukin-8; Leukocytes; Receptors, Complement; Receptors, Complement 3b

Topics: Anaphylaxis; Animals; Bronchial Spasm; Chemokines, C; Chemotactic Factors; Chemotactic Factors, Eosinophil; Chemotaxis, Leukocyte; Humans; Immunoglobulin E; Inflammation; Interleukin-8; Kinetics; Lymphokines; Mast Cells; Molecular Weight; Rats; Sialoglycoproteins

Topics: Administration, Intranasal; Airway Obstruction; Animals; Asthma; Bronchial Spasm; Chemotactic Factors; Clinical Trials as Topic; Cromolyn Sodium; Double-Blind Method; Guinea Pigs; Haplorhini; Histamine Release; Humans; Interleukin-8; Long-Term Care; Mast Cells; Sulfur Dioxide; Theophylline

The aim of this study was to assess the ability of nedocromil sodium (NS) to prevent the immediate asthmatic reaction and the increase in the serum level of heat stable neutrophil chemotactic activity (HS-NCA) induced by antigen inhalation. In a double-blind, cross-over study, 13 atopic subjects affected with seasonal asthma underwent a bronchial provocation test with a preselected dose of grass pollen allergen (enough to cause a decrease of > or = 20% in FEV1:FEV1 PD20) after pre-treatment with 4 mg NS or placebo. Serum samples were withdrawn from 11 subjects for HS-NCA determination. After NS administration the decrease in FEV1 was significantly less than after placebo administration at all time points after challenge (2 min P = 0.0004; 7 min, P = 0.0005; 17 min P = 0.0002 and 27 min P = 0.0005). The percentage increase in HS-NCA was significantly higher after placebo than after NS inhalation, both 10 (P = 0.0048) and 20 (P = 0.0068) min after challenge. Our study confirms previous investigations, showing that NS inhibits the immediate asthmatic response to allergen inhalation in atopic, asthmatic subjects and moreover it shows that this drug prevents in vivo the increase of the serum HS-NCA. This last finding has not been previously reported.

Topics: Adolescent; Adult; Asthma; Bronchial Provocation Tests; Bronchial Spasm; Chemotaxis, Leukocyte; Double-Blind Method; Female; Forced Expiratory Volume; Humans; Interleukin-8; Male; Middle Aged; Nedocromil; Neutrophils

Topics: Administration, Intranasal; Airway Obstruction; Animals; Asthma; Bronchial Spasm; Chemotactic Factors; Clinical Trials as Topic; Cromolyn Sodium; Double-Blind Method; Guinea Pigs; Haplorhini; Histamine Release; Humans; Interleukin-8; Long-Term Care; Mast Cells; Sulfur Dioxide; Theophylline

To assess the incidence of the late reaction of the bronchi in patients with atopic asthma the following methods of the provocation with atopic asthma the following methods of the provocation were applied: a) exercise test, b) a 3-minute ventilation with cold air and c) inhalation of the distilled water Disturbances of ventilation were assessed spirographically. An emphasis was also on the activity of NCF in the blood serum following the applied provocation tests. It was found that the late bronchospasm followed the exercise test in about half of the examined patients (48%). It was less frequent after hyperventilation with cold air (33%) and inhalation of the distilled water (38%). Bronchospasm was accompanied by the increase in NCF activity in the blood serum. The late bronchospasm after provocation tests in asthmatics is a real fact, not depending on the accidental ventilation disorders.

Topics: Adult; Asthma; Bronchial Provocation Tests; Bronchial Spasm; Female; Humans; Interleukin-8; Male

Topics: Air; Asthma; Bronchial Spasm; Chemotactic Factors; Cold Temperature; Humans; Hyperventilation; Interleukin-8; Physical Exertion

Adenosine, when it is administered by inhalation to asthmatic subjects, is a potent bronchoconstrictor, although its mechanism of action is not known. Since adenosine has been demonstrated to potentiate IgE-dependent mediator release from mast cells, we have investigated the possible relationship between adenosine-induced bronchoconstriction and release of mast cell mediators in 14 asthmatic subjects. In the first study the effect of the putative mast cell-stabilizing drug cromolyn sodium (SCG) was observed on the dose-related changes in SGaw and FEV1 produced by inhaled adenosine and histamine in seven subjects. Inhaled SCG (20 mg) had no effect on the airway responses to histamine. In contrast SCG significantly protected against adenosine-induced bronchoconstriction in four of the seven subjects as reflected by a decrease in the airway response to the highest concentrations of adenosine, from 65 +/- 8% to 12 +/- 3% (mean +/- SEM) for SGaw and 31 +/- 7% to 8 +/- 3% for FEV1. Those three subjects whose adenosine response was unaffected by SCG had received regular SCG until 12 hr before the studies. In a separate study on eight subjects, a single inhalation of adenosine, causing a maximum 61 +/- 4% fall in SGaw at 10 min, had no significant effect on circulating levels of histamine, neutrophil chemotactic factor, or cyclic AMP. Together these two studies suggest that bronchoconstriction produced by adenosine is not a consequence of enhanced mast cell-mediator release and that the inhibitory effects of SCG occur by a mechanism other than through mast cell stabilization.

Topics: Adenosine; Adult; Asthma; Bronchial Provocation Tests; Bronchial Spasm; Chemotactic Factors; Cromolyn Sodium; Cyclic AMP; Female; Forced Expiratory Volume; Histamine; Humans; Interleukin-8; Male; Mast Cells; Middle Aged

To determine whether neutrophils and monocytes are activated after allergen-induced asthma, changes in the expression of complement (C3b) receptors were measured by use of the rosette technique. There was a time-dependent increase in the percentages of neutrophil and monocyte rosettes in 13 asthmatic patients for up to 60 min after allergen-inhalation challenge. This was preceded by elevations in the concentrations of serum neutrophil chemotactic activity and reductions in the FEV1. These changes were not observed in seven asthmatic patients who had histamine-induced bronchoconstriction. The present findings support the view that inflammatory cells are activated after allergen-induced asthma and that this may be the result of the release of mast cell-associated mediators rather than the consequence of bronchoconstriction per se.

Topics: Adult; Allergens; Bronchial Spasm; Chemotactic Factors; Complement System Proteins; Female; Forced Expiratory Volume; Histamine; Humans; Interleukin-8; Macrophage Activation; Male; Monocytes; Neutrophils; Rosette Formation

Topics: Antigens; Asthma; Bronchial Spasm; Chemotactic Factors; Chemotactic Factors, Eosinophil; Humans; Hypersensitivity, Immediate; Immunoglobulin E; Interleukin-8; Lymphocytes; Mast Cells; Neutrophils

Topics: Albuterol; Antigens; Bronchial Spasm; Chemotactic Factors; Chemotaxis, Leukocyte; Cromolyn Sodium; Cytoplasmic Granules; Dose-Response Relationship, Drug; Forced Expiratory Volume; Humans; Interleukin-8; Mast Cells; Neutrophils; Sulfur Dioxide