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      Overexpression of chitotriosidase and YKL-40 in peripheral blood and sputum of healthy smokers and patients with chronic obstructive pulmonary disease

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          Despite 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.


          To examine peripheral blood and sputum chitotriosidase and YKL-40 expression in smokers and patients with COPD.


          Forty 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.


          Both 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.


          Our 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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          Most cited references 67

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          Chronic obstructive pulmonary disease.

           Chris Barnes (2000)
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            Studies on serum YKL-40 as a biomarker in diseases with inflammation, tissue remodelling, fibroses and cancer.

             Isik Johansen (2006)
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              YKL-40, a secreted glycoprotein, promotes tumor angiogenesis

              Tumor angiogenesis is of paramount importance in solid tumor development. Elevated serum levels of YKL-40, a secreted heparin-binding glycoprotein have been associated with a worse prognosis from a variety of advanced human cancers. Yet the role of YKL-40 activity in these cancers is still missing. Here, we have shown that ectopic expression of YKL-40 in MDA-MB-231 breast cancer cells and HCT-116 colon cancer cells led to larger tumor formation with an extensive angiogenic phenotype than did control cancer cells in mice. Affinity purified recombinant YKL-40 protein promoted vascular endothelial cell angiogenesis in vitro, the effects similar to the activities observed using MDA-MB-231 and HCT-116 cell conditioned medium after transfection with YKL-40. Further, YKL-40 was found to induce the coordination of membrane-bound receptor syndecan-1 and integrin αvβ3 and activate an intracellular signaling cascade including focal adhesion kinase and MAP kinase Erk1/2 in endothelial cells. Also, blockade of YKL-40 using siRNA gene knockdown suppressed tumor angiogenesis in vitro and in vivo. Immunohistochemical analysis of human breast cancer revealed a correlation between YKL-40 expression and blood vessel density. These findings provide novel insights into angiogenic activities and molecular mechanisms of YKL-40 in cancer development.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of Chronic Obstructive Pulmonary Disease
                22 July 2019
                : 14
                : 1611-1631
                [1 ]Department of Pneumology and Allergy, Medical University of Lodz , Lodz, Poland
                [2 ]Department of General and Oncological Pulmonology, Medical University of Lodz , Lodz, Poland
                [3 ]Department of Molecular Bases of Medicine, Medical University of Lodz , Lodz, Poland
                [4 ]Central Scientific Laboratory (CoreLab), Medical University of Lodz , Lodz, Poland
                Author notes
                Correspondence: Sebastian MajewskiDepartment of Pneumology and Allergy, Medical University of Lodz , 22 Kopcinskiego Street, 90-153Lodz, PolandFax +48 42 678 2129Email sebastian.majewski@
                © 2019 Majewski et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (

                Page count
                Figures: 9, Tables: 3, References: 78, Pages: 21
                Original Research

                Respiratory medicine

                chitotriosidase, chit1, ykl-40, chitinase, chitin-like protein, copd


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