title: Increases in eotaxin-positive cells in induced sputum from atopic asthmatic subjects after inhalational allergen challenge.
abstract: BACKGROUND
  Eosinophils are believed to be critical proinflammatory cells in airway mucosal damage in asthma. Eotaxin is a C-C chemokine with selective activity for eosinophils and basophils. Previous studies have shown increased expression of eotaxin in the airways of asthmatics at baseline. We aimed to investigate eotaxin expression during the late-phase reaction to allergen inhalation in atopic asthmatics.
  
  
  METHODS
  Sputum induction was performed before and 24 h after inhalational allergen challenge in atopic asthmatics, and eotaxin protein was detected immunocytochemically.
  
  
  RESULTS
  Thirteen patients with a mean decrease in forced expiratory volume in 1 s of 28% (+/-1.5) during the early asthmatic reaction, and 39% (+/-4.7) during the late asthmatic reaction produced sufficient sputum for study. The percentage of eosinophils in sputum was increased 24 h after allergen challenge (P<0.004), and eosinophil percentages in sputum after challenge correlated with the magnitude of the late-phase reaction (r=0.56, P=0.05). The percentage of eotaxin-positive cells increased from 12.6% (range 2-43.8) to 24.3% (8.1-47.1, P<0.005). Allergen-induced increases in eotaxin-positive cells correlated with increases in eosinophils (r=0.63, P<0.01).
  
  
  CONCLUSIONS
  These findings suggest that eotaxin may contribute to allergen-induced recruitment of eosinophils to the airway in asthmatic subjects.
authors.affiliation: Department of Allergy and Clinical Immunology, Imperial College School of Medicine (Royal Brompton Campus), National Heart and Lung Institute, London, UK.
authors.forename: K
authors.initials: K
authors.lastname: Zeibecoglou
authors.forename: A J
authors.initials: AJ
authors.lastname: Macfarlane
authors.forename: S
authors.initials: S
authors.lastname: Ying
authors.forename: Q
authors.initials: Q
authors.lastname: Meng
authors.forename: I
authors.initials: I
authors.lastname: Pavord
authors.forename: N C
authors.initials: NC
authors.lastname: Barnes
authors.forename: D S
authors.initials: DS
authors.lastname: Robinson
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D001985:Bronchial Provocation Tests; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000096:biosynthesis*; D004804:Eosinophils / Q000166:cytology*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007150:Immunohistochemistry; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013183:Sputum / Q000166:cytology* / Q000276:immunology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines