ABSTRACT
Objective To measure the levels of human interleukin (IL)-32 in the serum and induced sputum of patients with chronic obstructive pulmonary disease (COPD) and investigate the possible roles of IL-32 in COPD.Methods Sixty patients with acute exacerbation of COPD ( AECOPD),60 patients with stable COPD,and 30 healthy subjects were recruited.The concentrations of IL-8,tumor necrosis factor alpha (TNF-α),and IL-32 in serum and induced sputum were measured by enzyme-linked immunosorbent assay (ELISA).The correlations among IL-32,IL-8,TNF-α,and lung functions were investigated. The data were analyzed using a statistical software package (SPSS 13.0).Variables were compared with one-way ANOVA,and correlations among variables were analyzed using Pearson's correlation coefficient or Spearman's correlation coefficient.Results The serum IL-32 level was significantly higher in AECOPD patients [(175 ± 88) ng/L] than in healthy subjects [ (59 ± 21 ) ng/L] and in stable COPD patients [ (89 ± 34) ng/L] (P ＜ 0.05) ; the serum IL-32 level was also significantly higher in stable COPD patients than in healthy subjects (P ＜ 0.05).The sputum IL-32 level was significantly higher in AECOPD patients [ ( 163 ± 117) ng/L] than in healthy subjects [ ( 75 ± 38 ) ng/L] and stable COPD patients [ ( 108 ± 63 )ng/L] (P ＜0.05); the sputum IL-32 level was also significantly higher in stable COPD patients than in healthy subjects ( P ＜ 0.05 ).The sputum IL-32 level in AECOPD patients was positively correlated with the sputum IL-8 and TNF-α levels (r =0.49 and 0.53,respectively) (P ＜0.01 ).The sputum IL-32 level in AECOPD patients was negatively correlated with FEV1 predicted values,FEV1/FVC,and PaO2 (r =-0.44to -0.33) (P ＜ 0.01 ).The serum IL-32 level in AECOPD patients was positively correlated with the serum IL-8 and TNF-o levels (r =0.45 and 0.61,respectively) (P ＜ 0.01 ).The serum IL-32 level in AECOPD patients was negatively correlated with FEV1 predicted values,FEV1/FVC,and PaO2 (r =-0.46to - 0.29) ( P ＜ 0.01 ).Conclusions IL-32 may be involved in the pathogenesis of airway inflammation in COPD.IL-32 may be a useful marker of acute exacerbation of COPD.