Enhanced expression of interleukin-18 and its receptor in idiopathic pulmonary fibrosis

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Title
Enhanced expression of interleukin-18 and its receptor in idiopathic pulmonary fibrosis
Author(s)
Y Kitasato; T Hoshino; M Okamoto; S Kato; Y Koda; N Nagata; M Kinoshita; H Koga; Do Young Yoon; H Asao; H Ohmoto; T Koga; T Rikimaru; H Aizawa
Bibliographic Citation
American Journal of Respiratory Cell and Molecular Biology, vol. 31, no. 6, pp. 619-625
Publication Year
2004
Abstract
Idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP) is a major interstitial lung disease (ILD). Recently, we established a new mouse model for ILD in which daily administration of interleukin (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-18 receptor (IL-18R) α expression in the lungs of 18 patients with IPF/UIP and 13 control subjects by using monoclonal anti-IL-18 antibodies and a new monoclonal antibody for IL-18Rα (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 patients with IPF. IL-18Rα. was expressed in bronchoalveolar epithelium and alveolar macrophages in control subjects, and was strongly expressed in interstitial cells in patients with IPF, especially in the fibroblastic foci (FF). Interestingly, IL-18Rα expression was only weakly observed in areas showing established fibrosis. Semiquantitative analysis revealed that the histologic FF score was significantly correlated with the IL-18Rα expression level in FF lesions. Moreover, IL-18 levels in the serum and bronchoalveolar lavage fluid of patients with IPF were significantly higher than those in control subjects. Our findings suggest IL-18 and IL-18R are involved in the pathogenesis of IPF/ UIP.
ISSN
1044-1549
Publisher
Amer Thoracic Soc
DOI
http://dx.doi.org/10.1165/rcmb.2003-0306OC
Type
Article
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1. Journal Articles > Journal Articles
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