Abstract
Background: IL-18, identified as an IFN-γ–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-γ 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-γ level was significantly elevated in only pulmonary sarcoidosis (P < .001). In pulmonary sarcoidosis the IL-18 values significantly correlated with the IFN-γ 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. Conclusion: 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. (J Allergy Clin Immunol 2001;107:331-6.)
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