IL-18 production and pulmonary function in chronic obstructive pulmonary disease

¹ Division of Respirology, Neurology, and Rheumatology, Dept of Medicine, Kurume University School of Medicine, Kurume, Fukuoka 830-0011, Japan
² Division of Pathology and Cell Biology, Graduate School and Faculty of Medicine, University of the Ryukyus, Okinawa 903-0215, Japan
³ Dept of Pathology
⁴ 4th Dept of Internal Medicine, Fukuoka University School of Medicine, Fukuoka 811-0295, Japan

^* To whom correspondence should be addressed. E-mail: hoshino{at}med.kurume-u.ac.jp.

	Abstract

We analyzed IL-18 production and pulmonary function in patients with chronic obstructive pulmonary disease (COPD) to evaluate the role of IL-18 in COPD.

We used immunohistochemical techniques to examine IL-18 production in the lungs of patients with very severe COPD (GOLD Stage IV) (n=16), smokers (n=27), and non-smokers (n=23). Serum cytokine levels and pulmonary function were analyzed in patients with GOLD Stage I to IV COPD (n=62), smokers (n=34), and non-smokers (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 (P<0.05) higher than those in non-smokers. Moreover, serum levels of IL-18 in patients with GOLD Stage III and IV COPD were significantly (P<0.05) higher than in smokers and non-smokers. There was a significant negative correlation between serum IL-18 level and %FEV₁ in patients with COPD. In contrast, serum levels of IL-4, IL-13, and IFN- were not significantly increased in any of the three groups.

Overproduction of IL-18 in the lungs may be involved in the pathogenesis of COPD.

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