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Eur Respir J 2004; 24:49-56
Copyright ©ERS Journals Ltd 2004

CCL22 and CCL17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis

T. Inoue1, S. Fujishima2, E. Ikeda3, O. Yoshie4, N. Tsukamoto5, S. Aiso6, N. Aikawa2, A. Kubo5, K. Matsushima7 and K. Yamaguchi1

Depts of 1 Medicine, 2 Emergency & Critical Care Medicine, 3 Pathology, 5 Radiology, and 6 Anatomy, School of Medicine, Keio University, 4 Dept of Microbiology, Kinki University School of Medicine, Osaka, and 7 Dept of Molecular Preventive Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

CORRESPONDENCE: S. Fujishima, Dept of Emergency & Critical Care Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: fujishim@sc.itc.keio.ac.jp. Fax: 81 353633285

Keywords: Bronchoalveolar lavage, CC chemokine receptor 4, CCL17, CCL22, idiopathic pulmonary fibrosis, type-2 T-helper cell

Received: October 2, 2003
Accepted February 10, 2004

This study was supported, in part, by grants-in-aid from the Japanese Ministry of Education, Culture, Sports, Science and Technology, and the Keio Gijuku Fukuzawa Memorial Fund for the Advancement of Education and Research (both Tokyo, Japan).

Pulmonary fibrosis is caused by various known and unknown aetiologies, but the key pathogenic mechanisms are still ill-defined. Chemokines are a large family of chemotactic cytokines that play pivotal roles in various inflammatory diseases.

In the present study, the roles of chemokines in a rat model of radiation pneumonitis/pulmonary fibrosis were examined.

Accumulation of inflammatory cells and pneumonitis were observed on day 28, and diffuse alveolar wall thickening with extensive fibrosis was observed on day 56. In addition to the previously reported CCL2 (macrophage chemoattractant protein-1) induction, selective upregulation of CCL22 (macrophage-derived chemokine) and CCL17 (thymus and activation-regulated chemokine) were demonstrated for the first time in the irradiated lung tissues. Immunohistochemically, it was demonstrated that CCL22 and CCL17 were localised primarily to alveolar macrophages, whereas their receptor CC chemokine receptor 4 (CCR4) was detected on alveolar lymphocytes and macrophages. On further analysis of bronchoalveolar lavage fluid from patients with idiopathic pulmonary fibrosis and sarcoidosis, elevated levels of CCL22, but not of CCL17, were observed in the idiopathic pulmonary fibrosis patients.

Since these two chemokines play pivotal roles in various type-2 T-helper cell-dominant diseases, it was speculated that CCL22, and probably CCL17, are involved in the pathophysiology of radiation pneumonitis/pulmonary fibrosis and idiopathic pulmonary fibrosis through the recruitment of CC chemokine receptor 4-positive type-2 T-helper cells and alveolar macrophages.




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