• Sebastian Majewski, Damian Tworek, Karolina Szewczyk, Justyna Kiszałkiewicz, Zofia Kurmanowska, Ewa Brzeziańska-Lasota, Hanna Jerczyńska, Adam Antczak, Wojciech Jerzy Piotrowski, and Paweł Górski.
• Department of Pneumology and Allergy, Medical University of Lodz, Lodz, Poland.
• Int J Chron Obstruct Pulmon Dis. 2019 Jan 1; 14: 1611-1631.

BackgroundDespite the absence of endogenous chitin in humans, chitinases are present in the serum of healthy subjects and their levels are increased in a variety of chronic inflammatory conditions. It has been shown that chitotriosidase and structurally related chitinase-like protein-YKL-40 contribute to the pathogenesis of COPD. However, details regarding the relation of their systemic and local airways levels remain unknown.ObjectivesTo examine peripheral blood and sputum chitotriosidase and YKL-40 expression in smokers and patients with COPD.MethodsForty patients with COPD, 20 healthy smokers and 10 healthy never-smokers were studied. Serum and induced sputum chitotriosidase protein and activity levels, YKL-40 concentrations, and their gene expression in sputum cells and peripheral blood mononuclear cells (PBMC) were evaluated.ResultsBoth chitotriosidase protein levels and activity were higher in sputum obtained from COPD subjects compared to healthy never-smokers (P<0.05 and P<0.01, respectively). A similar pattern was observed for PBMC chitotriosidase mRNA expression (P<0.001). YKL-40 serum concentrations were elevated in healthy smokers and COPD subjects compared to healthy never-smokers (P<0.001 and P<0.01, respectively). In sputum, YKL-40 levels were increased in COPD compared to healthy never-smokers (P<0.01). PBMC YKL-40 mRNA expression was increased in COPD and healthy smokers compared to healthy never-smokers (P<0.0001). No associations were found between chitotriosidase or YKL-40 peripheral blood levels and sputum levels.ConclusionsOur results demonstrate that chitotriosidase and YKL-40 are overexpressed in peripheral blood and airways in both healthy smokers and COPD subjects which may indicate smoking-related activation of macrophages, neutrophils, and epithelial cells.

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