title: Comparison of plasma eotaxin family level in aspirin-induced and aspirin-tolerant asthma patients.
abstract: OBJECTIVE
  Eosinophilic infiltration of airway tissue is a central feature of aspirin-induced asthma (AIA). Eotaxins belong to the family of CC chemokines, which coordinate the recruitment of inflammatory cells bearing chemokine (C-C motif) receptor-3 to sites of allergic inflammation. In the present study, the levels of eotaxin-1, eotaxin-2, and eotaxin-3 following an oral aspirin provocation test (APT) were measured, and the relationship between the eotaxin level and clinical parameters in patients with asthma was evaluated.
  
  
  METHODS
  An APT was performed in patients with asthma. Twenty AIA patients and 23 aspirin-tolerant asthma (ATA) patients were identified. Plasma levels of eotaxin-1, eotaxin-2, and eotaxin-3 levels were measured by enzyme-linked immunosorbent assay in the 43 patients with asthma and in 39 control subjects.
  
  
  RESULTS
  The proportion of blood eosinophils was significantly higher in asthmatic patients than in control subjects. Nasal polyps were more common in AIA patients than in ATA patients (p < 0.05). In addition, the eotaxin-1 level was higher in AIA and ATA patients than in control subjects (p < 0.01 for each). The eotaxin-2 level was higher in ATA patients than in either the AIA patients (p < 0.05) or control subjects (p < 0.01). Similarly, the eotaxin-3 level was higher in ATA patients than in control subjects. A trend toward higher plasma levels of eotaxin-1 and eotaxin-3 at baseline and at 4 h after APT administration in the ATA group was noted but was not significant. Eotaxin-2 was also higher in ATA patients than in AIA patients at baseline and at 4 h after the APT.
  
  
  CONCLUSIONS
  This study shows that eotaxin-2 is differentially secreted in patients with asthma according to aspirin intolerance, and that secretion is not time-dependent in response to the APT in AIA and ATA patients. It therefore appears that eotaxin-2 may be up-regulated and may act differentially in patients with ATA.
authors.affiliation: Division of Allergy and Respiratory Diseases, Genome Research Center for Allergy and Respiratory Diseases, Soonchunhyang University, Bucheon Hospital, Gyeonggi Do, Korea.
authors.forename: Ji-Won
authors.initials: JW
authors.lastname: Min
authors.forename: An-Soo
authors.initials: AS
authors.lastname: Jang
authors.forename: Se-Min
authors.initials: SM
authors.lastname: Park
authors.forename: Seung-Ha
authors.initials: SH
authors.lastname: Lee
authors.forename: June-Hyuk
authors.initials: JH
authors.lastname: Lee
authors.forename: Sung-Woo
authors.initials: SW
authors.lastname: Park
authors.forename: Choon-Sik
authors.initials: CS
authors.lastname: Park
mesh_terms: D000328:Adult; D001241:Aspirin / Q000009:adverse effects; D001249:Asthma / Q000097:blood* / Q000139:chemically induced; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000097:blood* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000097:blood; D015854:Up-Regulation / Q000502:physiology
chemical_list: C515456:CCL11 protein, human; C515484:CCL24 protein, human; C120429:CCL26 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC; D001241:Aspirin