title: Upregulation of CD11b on eosinophils in aspirin induced asthma.
abstract: BACKGROUND
  Although a challenge test using non-steroidal anti-inflammatory drugs (NSAIDs) is crucial for diagnosis of aspirin-induced asthma (AIA), it also has drawbacks in terms of possible side effects. Therefore, alternative in-vitro diagnostic methods for AIA are awaited.
  
  
  METHODS
  Nineteen stable non-AIA patients (9 males and 10 females; mean age, 49.4 ± 4.8 years), and 20 AIA patients (9 males and 11 females; mean age, 51.1 ± 4.8 years) were enrolled in this study. CD11b and CD16 expressions on the peripheral-blood granulocytes after administration of aspirin and different concentrations of PGE2 in vitro were examined using flowcytometry.
  
  
  RESULTS
  Aspirin induced a significant increase in CD11b expression on eosinophils (CD16 negative granulocytes) in 19 AIA patients and one non-AIA patient. Increase in CD11b expression on eosinophils by aspirin administration was suppressed by PGE2 in a dose-dependent manner.
  
  
  CONCLUSIONS
  The measurement of CD11b expression on peripheral-blood eosinophils showed very high sensitivity and specificity of (-95%) in diagnosing AIA. Although this method requires laboratory facilities for flowcytometry, it may be very useful in diagnosis of AIA without side effects. In addition, PGE2 may be involved in regulation of CD11b expression on eosinophils by aspirin administration.
authors.affiliation: Division of Respiratory Medicine and Clinical Allergy, Department of Internal Medicine, Fujita Health University School of Medicine, Aichi 470-1192, Japan. isogai@fujita−hu.ac.jp
authors.forename: Sumito
authors.initials: S
authors.lastname: Isogai
authors.forename: Masamichi
authors.initials: M
authors.lastname: Hayashi
authors.forename: Naoki
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Mariko
authors.initials: M
authors.lastname: Morishita
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Minezawa
authors.forename: Takuya
authors.initials: T
authors.lastname: Okamura
authors.forename: Tami
authors.initials: T
authors.lastname: Hoshino
authors.forename: Mitsushi
authors.initials: M
authors.lastname: Okazawa
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Imaizumi
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000494:pharmacology; D001241:Aspirin / Q000009:adverse effects* / Q000494:pharmacology; D055963:Asthma, Aspirin-Induced / Q000097:blood* / Q000175:diagnosis; D039481:CD11b Antigen / Q000096:biosynthesis*; D015232:Dinoprostone / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005260:Female; D058851:GPI-Linked Proteins / Q000096:biosynthesis; D006801:Humans; D008297:Male; D008875:Middle Aged; D017452:Receptors, IgG / Q000096:biosynthesis; D015854:Up-Regulation / Q000187:drug effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D039481:CD11b Antigen; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; C509295:ITGAM protein, human; D017452:Receptors, IgG; D015232:Dinoprostone; D001241:Aspirin