title: Interleukin-18 levels in induced sputum are reduced in asthmatic and normal smokers.
abstract: BACKGROUND
  IL-18 is a cytokine which is known to have an important role in the development of a Th1 lymphocyte response. As such, it may have a regulatory role in asthma by modifying Th2 lymphocyte responses. Cigarette smoking may amplify the airway inflammation associated with asthma.
  
  
  OBJECTIVE
  This study investigated if IL-18 could be detected in induced sputum from asthmatics and normal subjects and if smoking altered IL-18 levels.
  
  
  METHODS
  Induced sputum was obtained from asthmatic (31 smokers, 35 non-smokers) and normal (20 smokers, 20 non-smokers) subjects. All smokers had a smoking history of > or =15 pack years. IL-18 levels in sputum supernatant were measured by ELISA. IL-18 mRNA expression and cellular localization were assessed by quantitative PCR and immunocytochemistry, respectively.
  
  
  RESULTS
  Smoking was associated with a significant reduction in IL-18 levels (median (interquartile range) - smokers 20 (0-102) pg/mL vs. non-smokers 358 (50-876) pg/mL, P<0.001). This was more pronounced in asthmatics (smokers, 47 (40-64) pg/mL vs. non-smokers, 530 (30-1484) pg/mL; P<0.001) than in normal subjects (smokers, 25 (0-78) pg/mL vs. non-smokers, 247 (50-656) pg/mL; P<0.01). Within each of the smoking and non-smoking groups there was no significant difference in IL-18 levels between asthmatic and normal subjects. There was no correlation between sputum IL-18 levels and any specific cell type in the sputum samples nor serum IgE levels. IL-18 mRNA expression was reduced in asthmatic smokers compared with non-smokers. IL-18 production was localized to sputum macrophages by immunocytochemistry.
  
  
  CONCLUSIONS
  IL-18 is detectable in induced sputum samples from both asthmatic and normal subjects. Cigarette smoking significantly reduces sputum IL-18 levels. This effect is more pronounced in asthmatics than in normal subjects.
authors.affiliation: Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK.
authors.forename: A
authors.initials: A
authors.lastname: McKay
authors.forename: M
authors.initials: M
authors.lastname: Komai-Koma
authors.forename: K J
authors.initials: KJ
authors.lastname: MacLeod
authors.forename: C C
authors.initials: CC
authors.lastname: Campbell
authors.forename: S M
authors.initials: SM
authors.lastname: Kitson
authors.forename: R
authors.initials: R
authors.lastname: Chaudhuri
authors.forename: L
authors.initials: L
authors.lastname: Thomson
authors.forename: C
authors.initials: C
authors.lastname: McSharry
authors.forename: F Y
authors.initials: FY
authors.lastname: Liew
authors.forename: N C
authors.initials: NC
authors.lastname: Thomson
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D020382:Interleukin-18 / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000276:immunology*; D013048:Specimen Handling / Q000379:methods; D013183:Sputum / Q000737:chemistry*
chemical_list: D020382:Interleukin-18