• Tianwen Lai, Dong Wu, Min Chen, Chao Cao, Zhiliang Jing, Li Huang, Yingying Lv, Xuanna Zhao, Quanchao Lv, Yajun Wang, Dongming Li, Bin Wu, and Huahao Shen.
• Department of Respiratory and Critical Care Medicine, Affiliated Hospital, Institute of Respiratory Diseases, Guangdong Medical College, Zhanjiang, China.
• Resp Res. 2016 Mar 24; 17: 31.

BackgroundRecent studies suggest that YKL-40, also called chitinase-3-like-1 protein, has been implicated in the pathogenesis of various inflammatory diseases. It is currently unknown, however, whether YKL-40 plays a role in acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and airway remodeling.MethodsWe evaluated serum YKL-40 levels in patients with AECOPD (n = 37) and stable COPD (n = 44), as well as in controls (n = 47). The association between YKL-40 expression and airway remodeling was analyzed. The effects of YKL-40 on collagen synthesis of primary human lung fibroblasts were also evaluated.ResultsSerum YKL-40 levels were elevated at AECOPD onset as compared to stable disease (median [interquartile range], 78.6 [52.3-122.2] ng/ml versus 46.7 [31.2-75.5] ng/ml; p = 0.0005). The ideal cutoff point for distinguishing patients with AECOPD from those with stable COPD was 64.7 ng/ml (AUC: 0.71; 95%CI: 0.596 to 0.823). YKL-40 expression correlated with airflow obstruction, C-reactive protein, and collagen deposition. Stimulation with YKL-40 promoted collagen production in lung fibroblasts through ERK- and p38-dependent mechanisms.ConclusionsYKL-40 expression is up-regulated in patients with COPD and correlates with exacerbation attacks and may contribute to airway remodeling by acting on lung fibroblasts. The current data may provide insight into the underlying pathogenesis of COPD, in which YKL-40 has an important pathogenic role.Trial RegistrationChiCTR-OCC-13003567.

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