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

Abstract

Background

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.

Objectives

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

Methods

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.

Results

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.

Conclusions

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.

Journal

Journal ID (nlm-ta): Int J Chron Obstruct Pulmon Dis

Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis

Journal ID (publisher-id): COPD

Journal ID (pmc): copd

Title: International Journal of Chronic Obstructive Pulmonary Disease

Publisher: Dove

ISSN (Print): 1176-9106

ISSN (Electronic): 1178-2005

Publication date (Electronic): 22 July 2019

Publication date Collection: 2019

Volume: 14

Pages: 1611-1631

Affiliations

[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 [phone]Email sebastian.majewski@ 123456umed.lodz.pl

Article

Publisher ID: 184097

DOI: 10.2147/COPD.S184097

PMC ID: 6660640

Copyright statement: © 2019 Majewski et al.

License:

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Page count

Figures: 9, Tables: 3, References: 78, Pages: 21

Categories

Subject: Original Research