Department of Respiratory Medicine, Medical School, University of Athens, Sotiria Hospital for Diseases of Chest, 152 Mesogion Avenue, Athens GR-11527, Greece.
Respir Med. 2009 Jul;103(7):1056-62. doi: 10.1016/j.rmed.2009.01.011. Epub 2009 Feb 8.
It has been shown that interleukin (IL)-18 levels in induced sputum are reduced in asthmatic and healthy smokers. However, in chronic obstructive pulmonary disease (COPD) patients, recent data show an overproduction in the lungs and increased serum levels of IL-18, suggesting that IL-18 may be involved in the pathogenesis of COPD.
In order to assess the relation of IL-18 with pulmonary function and airway inflammation in COPD, IL-18, tumour necrosis factor-alpha, and IL-8 levels were measured by ELISA in sputum supernatants obtained from patients with bronchitis type COPD (n=28), and healthy subjects (18 smokers and 17 non-smokers). Cellular localization of IL-18 was assessed by immunocytochemistry.
The levels of IL-18 were significantly higher in sputum supernatants of COPD patients compared to healthy smokers and non-smokers (p<0.05). IL-18 production was localized to sputum macrophages. IL-18 levels were inversely correlated with FEV(1) (% predicted) (r=-0.572, p=0.002) and FEV(1)/FVC ratio in COPD smokers (r=-0.608, p=0.001). No correlations were found between IL-18 levels and inflammatory markers studied in induced sputum obtained from COPD patients, healthy smokers and non-smokers.
In patients with COPD, increased levels of IL-18 in induced sputum were associated with airflow limitation, suggesting that IL-18 may be implicated in the pathogenesis of COPD.
已经表明，在哮喘和健康吸烟者中，诱导痰中的白细胞介素（IL）-18 水平降低。然而，在慢性阻塞性肺疾病（COPD）患者中，最近的数据显示肺部过度产生并增加血清中 IL-18 的水平，这表明 IL-18 可能参与 COPD 的发病机制。
为了评估 IL-18 与 COPD 患者肺功能和气道炎症的关系，通过 ELISA 测定了来自支气管炎型 COPD 患者（n=28）和健康受试者（18 名吸烟者和 17 名非吸烟者）的痰上清液中的 IL-18、肿瘤坏死因子-α和 IL-8 水平。通过免疫细胞化学评估 IL-18 的细胞定位。
与健康吸烟者和非吸烟者相比，COPD 患者的痰上清液中 IL-18 水平显著升高（p<0.05）。IL-18 的产生定位于痰巨噬细胞。IL-18 水平与 COPD 吸烟者的 FEV1（%预计值）（r=-0.572，p=0.002）和 FEV1/FVC 比值呈负相关（r=-0.608，p=0.001）。在 COPD 患者、健康吸烟者和非吸烟者的诱导痰中，未发现 IL-18 水平与所研究的炎症标志物之间存在相关性。
在 COPD 患者中，诱导痰中 IL-18 水平升高与气流受限相关，这表明 IL-18 可能与 COPD 的发病机制有关。
