Increased expression of YKL-40, a chitinase-like protein, in serum and lung of patients with idiopathic pulmonary fibrosis

Kazuki Furuhashi, Takafumi Suda, Yutaro Nakamura, Naoki Inui, Dai Hashimoto, Seiichi Miwa, Hiroshi Hayakawa, Hideki Kusagaya, Yutaka Nakano, Hirotoshi Nakamura, Kingo Chida, Kazuki Furuhashi, Takafumi Suda, Yutaro Nakamura, Naoki Inui, Dai Hashimoto, Seiichi Miwa, Hiroshi Hayakawa, Hideki Kusagaya, Yutaka Nakano, Hirotoshi Nakamura, Kingo Chida

Abstract

Background: YKL-40, a mammalian member of chitinase-like proteins, has been shown to play a role in pathological conditions leading to tissue remodeling and fibrosis. Recently, YKL-40 was found to be increased in severe asthma, suggesting that YKL-40 contributes to airway remodeling; however, no data are available about YKL-40 expression in idiopathic pulmonary fibrosis (IPF). The present study was conducted to investigate YKL-40 expression in the serum and lung of IPF patients, and to determine its clinical significance.

Methods: Using an enzyme-linked immunosorbent assay, we measured YKL-40 levels in the serum of 63 IPF patients and in bronchoalveolar lavage fluid (BALF) of 18 IPF patients. YKL-40 levels were also assessed in the serum and BALF of healthy subjects. We further investigated the relationship between serum YKL-40 levels and clinical parameters. Additionally, immunohistochemical staining for YKL-40 was performed in lung specimens of IPF patients and control subjects.

Results: Serum and BALF YKL-40 levels were significantly higher in IPF than in controls (serum: 245.8+/-180.2ng/ml vs. 116.0+/-58.3ng/ml; BALF: 17.8+/-19.1ng/ml vs. 0.3+/-0.9ng/ml, respectively). Serum YKL-40 levels significantly correlated positively with serum KL-6 levels and AaDO(2), and negatively with DLco and PaO(2). Immunohistochemical study revealed enhanced YKL-40 expression in alveolar macrophages and bronchiolar epithelia adjacent to fibrotic lesions in IPF, but not in controls.

Conclusions: These data suggest that YKL-40 is increased in the circulation and lungs of IPF patients, suggesting that this glycoprotein is associated with the pathophysiology of IPF.

Copyright 2010 Elsevier Ltd. All rights reserved.

Source: PubMed

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