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Published ahead of print on August 12, 2004, doi:10.1165/rcmb.2003-0306OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 619-625

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Submitted on August 20, 2003
Revised on August 12, 2004

Enhanced Expression of IL-18 and its Receptor in Idiopathic Pulmonary Fibrosis

Yasuhiko Kitasato1, Tomoaki Hoshino1*, Masaki Okamoto2, Seiya Kato3, Yoshiro Koda4, Nobuhiko Nagata5, Masaharu Kinoshita6, Hideyuki Koga2, Do-Young Yoon7, Hironobu Asao8, Hiroshi Ohmoto9, Takeharu Koga1, Toru Rikimaru1, and Hisamichi Aizawa1

1 Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan, 2 Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan; Department of Respiratory Medicine, National Kyushu Medical Center, Fukuoka, Fukuoka, Japan, 3 Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan, 4 Department of Forensic Medicine, Kurume University School of Medicine, Kurume, Fukuoka, Japan, 5 Department of Respiratory Medicine, National Omuta Hospital, Omuta, Fukuoka, Japan, 6 Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan; Nagata Hospital, Yanagawa, Fukuoka, Japan, 7 Laboratory Cellular Biology, Korea Research Institute, Taejon, Korea, Republic of, 8 Department of Microbiology and Immunology, Tohoku University School of Medicine, Sendai, Miyagi, Japan, 9 Carna Biosciences Inc., Kobe, Hyogo, Japan

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

Idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP) is a major interstitial lung disease (ILD). Recently, we established a new mouse model for ILD in which daily administration of IL-18 with IL-2 induces lethal lung injury, suggesting that IL-18 is involved in the pathogenesis of ILD. Here, utilizing immunohistochemistry, we have analyzed IL-18 and IL-18R{alpha} expression in the lungs of 18 IPF/UIP patients and 13 control subjects by using monoclonal anti-IL-18 antibodies and a new monoclonal antibody for IL-18R{alpha} (H44). IL-18 was expressed in bronchoalveolar epithelium, alveolar macrophages, and the endothelium of small vessels in control subjects, and was abundantly expressed in the majority of pulmonary cells in IPF patients. IL-18R{alpha} was expressed in bronchoalveolar epithelium and alveolar macrophages in control subjects, and was strongly expressed in interstitial cells in IPF patients, especially in the fibroblastic foci (FF). Interestingly, IL-18R{alpha} expression was only weakly observed in areas showing established fibrosis. Semiquantitative analysis revealed that the histological FF score was significantly correlated with the IL-18R{alpha} expression level in FF lesions. Moreover, IL-18 levels in the serum and bronchoalveolar lavage fluid of IPF patients were significantly higher than those in control subjects. Our findings suggest IL-18 and IL-18R are involved in the pathogenesis of IPF/UIP.




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