title: Inflammatory cell number and mediators in bronchoalveolar lavage fluid and peripheral blood in subjects with asthma with increased nocturnal airways narrowing.
abstract: BACKGROUND
  Increased nocturnal airways narrowing (NAN) in asthma is thought to occur as the result of intensification of inflammatory processes in the airways. In this study we investigated the presence of inflammatory cells and mediators in bronchoalveolar lavage (BAL) fluid and peripheral blood (PB) and assessed their relationship with the occurrence of increased NAN.
  
  
  METHODS
  BAL fluid and PB samples were assessed at 16:00 and 04:00 hours, separated by 7 days or more, in eight nonatopic healthy subjects (group 1) and 17 atopic subjects with asthma who were using inhaled bronchodilators only. The latter subjects were prospectively assigned to groups with and without NAN, as defined by a mean circadian peak expiratory flow variation of less than 15% (group 2) and 15% or more (group 3), respectively.
  
  
  RESULTS
  Significantly higher eosinophil numbers and inflammatory activation products (eosinophil cationic protein, eosinophil-derived neurotoxin, histamine) were found in BAL fluid and PB from subjects with asthma in comparison with control subjects. However, increased NAN was not generally associated with a circadian fluctuation in cell number and inflammatory mediators in BAL fluid and PB. No differences in inflammatory cell numbers existed that distinguished between groups 2 and 3. However, in group 3 significantly higher BAL prostaglandin D2 levels (70 vs 24 pg/ml; range, 28 to 102 vs 11 to 90 pg/ml; p = 0.04) and serum eosinophil cationic protein levels (17.6 vs 16.1 ng/ml; range, 6.3 to 17.5 vs 6.3 to 60.3 ng/ml; p = 0.03) at 16:00 hours were detected compared with group 2.
  
  
  CONCLUSIONS
  Our findings suggest that increased NAN is more likely to occur in subjects with asthma with ongoing increased cellular activation during the day.
authors.affiliation: Department of Pulmonology, University Hospital, Groningen, The Netherlands.
authors.forename: Y
authors.initials: Y
authors.lastname: Oosterhoff
authors.forename: H F
authors.initials: HF
authors.lastname: Kauffman
authors.forename: B
authors.initials: B
authors.lastname: Rutgers
authors.forename: F J
authors.initials: FJ
authors.lastname: Zijlstra
authors.forename: G H
authors.initials: GH
authors.lastname: Koëter
authors.forename: D S
authors.initials: DS
authors.lastname: Postma
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000473:pathology / Q000503:physiopathology*; D001798:Blood Proteins / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology*; D002940:Circadian Rhythm; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000502:physiology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010366:Peak Expiratory Flow Rate; D012260:Ribonucleases
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D012260:Ribonucleases