title: In vivo uptake of inhaled particles by airway phagocytes is enhanced in patients with mild asthma compared with normal volunteers.
abstract: BACKGROUND
  The uptake of inhaled particulate matter by airway phagocytes is an important defence mechanism contributing to the clearance of potentially toxic substances, including aeroallergens, from the lung. Since airway monocytes and macrophages can also function as antigen presenting cells, their ability to engulf materials deposited on the airway surface is of particular interest in patients with allergic asthma. To determine whether airway mononuclear phagocytes of patients with allergic asthma might have enhanced phagocytic activity, the in vivo uptake of inhaled radiolabelled particles was compared in 10 patients with mild allergic asthma and 8 healthy (non-allergic) individuals.
  
  
  METHODS
  Phagocyte function was assessed by quantifying the proportion of radioactivity associated with cellular and supernatant fractions of induced sputum 2 h after inhalation of radiolabelled sulfur colloid particles. All subjects were pretreated with albuterol before sputum induction. A standardised breathing pattern was used to target aerosol deposition in the bronchial airways.
  
  
  RESULTS
  In vivo particle uptake by airway cells was significantly greater in patients with asthma than in healthy volunteers (57.2% (95% CI 46.5% to 67.9%) vs 22.3% (95% CI 4.9% to 39.6%), p<0.01), as was in vitro phagocytosis of opsonised zymosan-A bioparticles. There was also a significant correlation (r = 0.85, p<0.01) between the percentage of sputum mononuclear phagocytes and the percentage uptake of particles in the patients with asthma but not in the control subjects.
  
  
  CONCLUSIONS
  In vivo particle uptake by airway macrophages is enhanced in persons with mild asthma. Enhanced uptake and processing of particulate antigens could contribute to the pathogenesis and progression of allergic airways disease and may contribute to the increased risk of disease exacerbation associated with particulate exposure.
authors.affiliation: Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, Chapel Hill, NC 27599-7310, USA. jcl@med.unc.edu
authors.forename: J C
authors.initials: JC
authors.lastname: Lay
authors.forename: N E
authors.initials: NE
authors.lastname: Alexis
authors.forename: K L
authors.initials: KL
authors.lastname: Zeman
authors.forename: D B
authors.initials: DB
authors.lastname: Peden
authors.forename: W D
authors.initials: WD
authors.lastname: Bennett
mesh_terms: D000328:Adult; D001249:Asthma / Q000378:metabolism*; D051940:B7-2 Antigen / Q000378:metabolism; D001980:Bronchi / Q000378:metabolism*; D002452:Cell Count; D003102:Colloids / Q000493:pharmacokinetics; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009079:Mucociliary Clearance / Q000502:physiology; D052638:Particulate Matter / Q000493:pharmacokinetics*; D010586:Phagocytes / Q000378:metabolism*; D016719:Radioimmunodetection; D017452:Receptors, IgG / Q000378:metabolism; D013183:Sputum / Q000166:cytology; D013457:Sulfur Compounds / Q000493:pharmacokinetics; D055815:Young Adult
chemical_list: D051940:B7-2 Antigen; D003102:Colloids; D052638:Particulate Matter; D017452:Receptors, IgG; D013457:Sulfur Compounds