Tanaka H, Miyazaki N, Oashi K, Teramoto S, Shiratori M, Hashimoto M, Ohmichi M, Abe S
Third Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
J Allergy Clin Immunol. 2001 Feb;107(2):331-6. doi: 10.1067/mai.2001.112275.
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.
The aim was to evaluate the contribution of IL-18 to asthma exacerbation.
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.
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.
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.
白细胞介素 -18（IL -18）被鉴定为一种γ干扰素诱导因子，是一种促炎细胞因子，在辅助性T细胞1（TH1）细胞激活中起重要作用。最近，有报道称组胺可诱导IL -18产生，且IL -18可能作为TH1和TH2细胞因子的协同诱导剂。
旨在评估IL -18在哮喘急性发作中的作用。
检测了稳定期哮喘患者（n = 28）、急性轻或中度哮喘患者（n = 23）、结节病患者（n = 35）以及健康受试者（n = 26）的血清IL -18、可溶性白细胞介素 -2受体、嗜酸性粒细胞阳离子蛋白和血浆γ干扰素水平，以及呼气峰值流速。我们比较了急性哮喘患者与缓解期患者的血清IL -18水平，并观察了哮喘治疗后急性发作期的时间进程。
急性哮喘患者（215±33 pg/mL，均值±标准误；P = 0.02）和结节病患者（239±27 pg/mL，P = 0.008）的血清IL -18水平显著高于对照组（127±11 pg/mL），但仅结节病患者的血浆γ干扰素水平显著升高（P < 0.001）。在结节病中，IL -18值与γ干扰素水平显著相关（r = 0.61，P < 0.001），但在急性哮喘中它们不相关。急性哮喘发作期的IL -18水平显著高于缓解期（P = 0.01）。在急性哮喘中，循环IL -18水平与血清可溶性白细胞介素 -2受体水平显著相关（r = 0.77，P < 0.0001），但与血清嗜酸性粒细胞阳离子蛋白水平无关。IL -18水平与呼气峰值流速呈负相关趋势。急性哮喘中升高的IL -18水平在治疗后第3天（P = 0.02）和第7天（P = 0.002）迅速下降。
提示IL -18可能在激活免疫反应中发挥潜在作用，并可能反映轻、中度哮喘发作时的疾病活动情况。
