title: Association of interleukin-5 and eotaxin with acute exacerbation of asthma.
abstract: BACKGROUND
  Airway eosinophilia is frequently observed during acute exacerbation of asthma. Interleukin-5 (IL-5) and eotaxin are directly involved in the airway eosinophilia found in persistent asthma. Interrelation between these cytokines is expected to occur in acute exacerbation of asthma. Thus, we evaluated the relevance of interaction between eotaxin and IL-5 in the airway inflammation of acute exacerbation.
  
  
  METHODS
  We measured the number of inflammatory cells and the amount of eotaxin and IL-5 in sputum from 22 healthy subjects, 21 asthmatics with acute exacerbation and 16 patients with mild persistent asthma, and reassessed these values in 7 subjects with acute exacerbation after 7 days' treatment with systemic steroid (2 mg/kg/day). Sources of IL-5 and eotaxin were investigated by immunohistochemical staining of sputum cells of 4 cases from each group.
  
  
  RESULTS
  Both IL-5 and eotaxin levels were higher in patients with acute exacerbation of asthma than in patients with persistent asthma and normal subjects. IL-5 and eotaxin levels were significantly correlated with eosinophil percentages in mild persistent asthma. Eotaxin staining was found mainly on macrophages and occasionally on eosinophils. Steroid treatment markedly decreased eosinophil percentages and IL-5 levels within 7 days but did not alter eotaxin levels.
  
  
  CONCLUSIONS
  Both IL-5 and eotaxin are associated with acute exacerbation of asthma. IL-5 rather than eotaxin is effectively decreased by the inhibitory effect of steroid in acute exacerbation.
authors.affiliation: Asthma and Allergy Research Group, Soonchunhyang University Hospital, Bucheon, Korea. mdcspark@unitel.co.kr
authors.forename: Sung Woo
authors.initials: SW
authors.lastname: Park
authors.forename: Do Jin
authors.initials: DJ
authors.lastname: Kim
authors.forename: Hun Soo
authors.initials: HS
authors.lastname: Chang
authors.forename: Sang Jun
authors.initials: SJ
authors.lastname: Park
authors.forename: Young Mok
authors.initials: YM
authors.lastname: Lee
authors.forename: Jai Soung
authors.initials: JS
authors.lastname: Park
authors.forename: Il Yup
authors.initials: IY
authors.lastname: Chung
authors.forename: June Hyuk
authors.initials: JH
authors.lastname: Lee
authors.forename: Choon-Sik
authors.initials: CS
authors.lastname: Park
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D019819:Budesonide / Q000627:therapeutic use; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000276:immunology* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000276:immunology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D015848:Interleukin-5 / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D013183:Sputum / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013224:Status Asthmaticus / Q000188:drug therapy / Q000276:immunology*
chemical_list: D000893:Anti-Inflammatory Agents; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D015848:Interleukin-5; D019819:Budesonide