Characteristics of peripheral blood eosinophils in patients with nocturnal asthma.

A number of mechanisms have been proposed to explain nocturnal exacerbations of asthma including circadian patterns in circulating cortisol and catecholamines. These factors may influence airway smooth muscle tone and circulating eosinophil characteristics and function. Because recent evidence has indicated that eosinophils contribute to airway inflammation and the severity of asthma, we evaluated the relationship among peripheral blood eosinophils, their density distribution, and the appearance of nocturnal asthma. Fifteen patients with asthma were evaluated. Spirometry (FEV1 and FVC) was determined at 0400 and 1600, and the number and density distribution of peripheral blood eosinophils were determined. Five patients had nocturnal asthma, defined as a 15% or greater fall in FEV1 at 0400 versus 1600. The patients with nocturnal asthma had greater numbers of eosinophils (cells x 10(6)/ml) at 0400 (0.845 +/- 0.13 versus 0.351 +/- 0.03) and 1600 (0.651 +/- 0.18 versus 0.319 +/- 0.07) and a greater circadian variation with peak eosinophilia at 0400. Furthermore, we found a significant circadian increase in low-density eosinophils (as determined by Percoll density gradient centrifugation) at 0400, but only in patients with nocturnal asthma. These observations suggest that a circadian variation in low density eosinophils may contribute to nocturnal exacerbations of asthma.

[1]  R. Martin,et al.  Circadian basis of the late asthmatic response. , 1990, The American review of respiratory disease.

[2]  J. Bousquet,et al.  Eosinophilic inflammation in asthma. , 1990, The New England journal of medicine.

[3]  W. Busse,et al.  Superoxide generation by hypodense eosinophils from patients with asthma. , 1990, The American review of respiratory disease.

[4]  A. Kay,et al.  Eosinophils and T-lymphocytes in late-phase allergic reactions. , 1990, The Journal of allergy and clinical immunology.

[5]  G. Gleich The eosinophil and bronchial asthma: current understanding. , 1990, The Journal of allergy and clinical immunology.

[6]  C. Wegner,et al.  Repeated antigen inhalation results in a prolonged airway eosinophilia and airway hyperresponsiveness in primates. , 1990, Journal of applied physiology.

[7]  W. Owen,et al.  IL-5-dependent conversion of normodense human eosinophils to the hypodense phenotype uses 3T3 fibroblasts for enhanced viability, accelerated hypodensity, and sustained antibody-dependent cytotoxicity. , 1989, Journal of immunology.

[8]  G Cuttitta,et al.  Relationship of nocturnal bronchoconstriction to sleep stages. , 1989, The American review of respiratory disease.

[9]  S. Holgate,et al.  Cellular events in the bronchi in mild asthma and after bronchial provocation. , 1989, The American review of respiratory disease.

[10]  T. Fukuda,et al.  Heterogeneity of human eosinophils. , 1989, The Journal of allergy and clinical immunology.

[11]  R. Kiani,et al.  Comparative, multicenter studies of cefixime and amoxicillin in the treatment of respiratory tract infections. , 1988, The American journal of medicine.

[12]  M. Turner-Warwick,et al.  Epidemiology of nocturnal asthma. , 1988, The American journal of medicine.

[13]  W. Owen,et al.  Human eosinophils have prolonged survival, enhanced functional properties, and become hypodense when exposed to human interleukin 3. , 1988, The Journal of clinical investigation.

[14]  T. Suda,et al.  Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor , 1988, The Journal of experimental medicine.

[15]  W. Busse,et al.  The presence of hypodense eosinophils and diminished chemiluminescence response in asthma. , 1988, The Journal of allergy and clinical immunology.

[16]  J. Gamble,et al.  Recombinant human interleukin 5 is a selective activator of human eosinophil function , 1988, The Journal of experimental medicine.

[17]  W. Owen,et al.  Regulation of human eosinophil viability, density, and function by granulocyte/macrophage colony-stimulating factor in the presence of 3T3 fibroblasts , 1987, The Journal of experimental medicine.

[18]  J. David,et al.  The regulation of human eosinophil function by cytokines. , 1987, Immunology today.

[19]  P. Barnes,et al.  Circadian variation in airway function. , 1985, The American journal of medicine.

[20]  M. Peters,et al.  Increased numbers of hypodense eosinophils in the blood of patients with bronchial asthma. , 1985, The American review of respiratory disease.

[21]  H. Sluiter,et al.  Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions. , 1985, The American review of respiratory disease.

[22]  H. Mita,et al.  Release of leukotriene C4 from human eosinophils and its relation to the cell density. , 1985, International archives of allergy and applied immunology.

[23]  M. Grunstein,et al.  Respiratory response to intraesophageal acid infusion in asthmatic children during sleep. , 1983, The Journal of allergy and clinical immunology.

[24]  W. Y. Chen,et al.  Airway cooling and nocturnal asthma. , 1982, Chest.

[25]  C. Dollery,et al.  Nocturnal asthma and changes in circulating epinephrine, histamine, and cortisol. , 1980, The New England journal of medicine.

[26]  D. Loegering,et al.  Cytotoxic effects of the guinea pig eosinophil major basic protein on tracheal epithelium. , 1980, Laboratory investigation; a journal of technical methods and pathology.

[27]  D. Pavia,et al.  The retention of lung secretions during the night in normal subjects. , 1978, Clinical science and molecular medicine. Supplement.

[28]  S. Spector,et al.  Standardization of bronchial inhalation challenge procedures. , 1975, The Journal of allergy and clinical immunology.

[29]  C. Soutar,et al.  Nocturnal and morning asthma. Relationship to plasma corticosteroids and response to cortisol infusion. , 1975, Thorax.

[30]  E D Robin,et al.  Total eosinophil counts in the management of bronchial asthma. , 1975, The New England journal of medicine.

[31]  A. Bøyum,et al.  Isolation of mononuclear cells and granulocytes from human blood. , 1968 .