title: IL-18 might reflect disease activity in mild and moderate asthma exacerbation.
abstract: BACKGROUND
  IL-18, identified as an IFN-gamma-inducing factor, is a proinflammatory cytokine that plays an important role in TH1 cell activation. Recently, it was reported that histamine induced IL-18 and that IL-18 might act as a coinducer of TH1 and TH2 cytokines.
  
  
  OBJECTIVE
  The aim was to evaluate the contribution of IL-18 to asthma exacerbation.
  
  
  METHODS
  Serum IL-18, soluble IL-2 receptor, eosinophil cationic protein, and plasma IFN-gamma levels, as well as peak expiratory flow were measured in patients with stable asthma (n = 28), acute mild or moderate asthma (n = 23), or pulmonary sarcoidosis (n = 35) and in healthy subjects (n = 26). We compared the serum IL-18 levels between patients with acute asthma and those in remission and examined the time course in acute exacerbation after asthma therapy.
  
  
  RESULTS
  Significantly higher serum IL-18 levels were found in patients with acute asthma (215 +/- 33 pg/mL, mean +/- SE; P = .02) and pulmonary sarcoidosis (239 +/- 27 pg/mL, P = .008) than in control subjects (127 +/- 11 pg/mL), but the plasma IFN-gamma level was significantly elevated in only pulmonary sarcoidosis (P < .001). In pulmonary sarcoidosis the IL-18 values significantly correlated with the IFN-gamma levels (r = 0.61, P < .001), but in acute asthma they did not. The IL-18 levels during acute asthma exacerbation were significantly higher (P = .01) than on remission days. In acute asthma, circulating IL-18 levels significantly correlated with serum soluble IL-2 receptor levels (r = 0.77, P < .0001) but not with serum eosinophil cationic protein levels. The IL-18 level had a tendency to inversely correlate with peak expiratory flow. The elevated IL-18 levels in acute asthma quickly decreased on day 3 (P = .02) and day 7 (P = .002) after therapy.
  
  
  CONCLUSIONS
  It was suggested that IL-18 may play a potential role to activate immunologic responses and may reflect disease activity in mild and moderate asthma exacerbation.
authors.affiliation: Third Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: N
authors.initials: N
authors.lastname: Miyazaki
authors.forename: K
authors.initials: K
authors.lastname: Oashi
authors.forename: S
authors.initials: S
authors.lastname: Teramoto
authors.forename: M
authors.initials: M
authors.lastname: Shiratori
authors.forename: M
authors.initials: M
authors.lastname: Hashimoto
authors.forename: M
authors.initials: M
authors.lastname: Ohmichi
authors.forename: S
authors.initials: S
authors.lastname: Abe
mesh_terms: D000208:Acute Disease; D000368:Aged; D001249:Asthma / Q000097:blood*; D001798:Blood Proteins / Q000032:analysis; D016207:Cytokines / Q000378:metabolism; D047091:Eosinophil Granule Proteins; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000097:blood; D020382:Interleukin-18 / Q000097:blood*; D008171:Lung Diseases / Q000097:blood; D008297:Male; D008875:Middle Aged; D010366:Peak Expiratory Flow Rate; D015375:Receptors, Interleukin-2 / Q000097:blood; D012260:Ribonucleases; D012507:Sarcoidosis / Q000097:blood; D012995:Solubility; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D001798:Blood Proteins; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D020382:Interleukin-18; D015375:Receptors, Interleukin-2; D007371:Interferon-gamma; D012260:Ribonucleases