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Interleukin-18 production and pulmonary function in COPD

¹ Division of Respirology, Neurology and Rheumatology, Dept of Medicine, Kurume University School of Medicine, Kurume, ³ Dept of Pathology and ⁴ 4th Dept of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, and ² Division of Pathology and Cell Biology, Graduate School and Faculty of Medicine, University of the Ryukyus, Okinawa, Japan.

CORRESPONDENCE: T. Hoshino, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume, Fukuoka 830-0011, Japan, Fax: 81 942317560. E-mail: hosino{at}med.kurume-u.ac.jp

Keywords: Chronic obstructive pulmonary disease, chronic obstructive pulmonary disease clinical/basic investigations, cytokine production

Received: February 16, 2007
Accepted October 24, 2007

Interleukin (IL)-18 production and pulmonary function were evaluated in patients with chronic obstructive pulmonary disease (COPD) in order to determine the role of IL-18 in COPD.

Immunohistochemical techniques were used to examine IL-18 production in the lungs of patients with very severe COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage IV, n = 16), smokers (n = 27) and nonsmokers (n = 23). Serum cytokine levels and pulmonary function were analysed in patients with GOLD stage I–IV COPD (n = 62), smokers (n = 34) and nonsmokers (n = 47).

Persistent and severe small airway inflammation was observed in the lungs of ex-smokers with very severe COPD. IL-18 proteins were strongly expressed in alveolar macrophages, CD8+ T-cells, and both the bronchiolar and alveolar epithelia in the lungs of COPD patients. Serum levels of IL-18 in COPD patients and smokers were significantly higher than those in nonsmokers. Moreover, serum levels of IL-18 in patients with GOLD stage III and IV COPD were significantly higher than in smokers and nonsmokers. There was a significant negative correlation between serum IL-18 level and the predicted forced expiratory volume in one second in patients with COPD. In contrast, serum levels of IL-4, IL-13 and interferon- were not significantly increased in any of the three groups.

In conclusion, overproduction of interleukin-18 in the lungs may be involved in the pathogenesis of chronic obstructive pulmonary disease.

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