title: Role of inflammation in nocturnal asthma.
abstract: BACKGROUND
  Nocturnal airway narrowing is a common problem for patients with asthma but the role of inflammation in its pathogenesis is unclear. Overnight changes in airway inflammatory cell populations were studied in patients with nocturnal asthma and in control normal subjects.
  
  
  METHODS
  Bronchoscopies were performed at 0400 hours and 1600 hours in eight healthy subjects and in 10 patients with nocturnal asthma (> 15% overnight fall in peak flow plus at least one awakening/week with asthma). The two bronchoscopies were separated by at least five days, and both the order of bronchoscopies and site of bronchoalveolar lavage (middle lobe or lingula with contralateral lower lobe bronchial biopsy) were randomised.
  
  
  RESULTS
  In the normal subjects there was no difference in cell numbers and differential cell counts in bronchoalveolar lavage fluid between 0400 and 1600 hours, but in the nocturnal asthmatic subjects both eosinophil counts (median 0.11 x 10(5) cells/ml at 0400 hours, 0.05 x 10(5) cells/ml at 1600 hours) and lymphocyte numbers (0.06 x 10(5) cells/ml at 0400 hours, 0.03 x 10(5) cells/ml at 1600 hours) increased at 0400 hours, along with an increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid (3.0 micrograms/ml at 0400 hours, 2.0 micrograms/l at 1600 hours). There were no changes in cell populations in the bronchial biopsies or in alveolar macrophage production of hydrogen peroxide, GM-CSF, or TNF alpha in either normal or asthmatic subjects at 0400 and 1600 hours. There was no correlation between changes in overnight airway function and changes in cell populations in the bronchoalveolar lavage fluid.
  
  
  CONCLUSIONS
  This study confirms that there are increases in inflammatory cell populations in the airway fluid at night in asthmatic but not in normal subjects. The results have also shown a nocturnal increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid, but these findings do not prove that these inflammatory changes cause nocturnal airway narrowing.
authors.affiliation: Department of Medicine (RIE), University of Edinburgh, UK.
authors.forename: T W
authors.initials: TW
authors.lastname: Mackay
authors.forename: W A
authors.initials: WA
authors.lastname: Wallace
authors.forename: S E
authors.initials: SE
authors.lastname: Howie
authors.forename: P H
authors.initials: PH
authors.lastname: Brown
authors.forename: A P
authors.initials: AP
authors.lastname: Greening
authors.forename: M K
authors.initials: MK
authors.lastname: Church
authors.forename: N J
authors.initials: NJ
authors.lastname: Douglas
mesh_terms: D000328:Adult; D001249:Asthma / Q000209:etiology* / Q000503:physiopathology; D001798:Blood Proteins; D001992:Bronchoalveolar Lavage Fluid; D002940:Circadian Rhythm / Q000502:physiology*; D047091:Eosinophil Granule Proteins; D004804:Eosinophils; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation; D007958:Leukocyte Count; D008214:Lymphocytes; D016676:Macrophages, Alveolar / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils; D010366:Peak Expiratory Flow Rate; D011897:Random Allocation; D012260:Ribonucleases
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D012260:Ribonucleases