Association between Galectin-13 Expression and Eosinophilic Airway Inflammation in Chronic Obstructive Pulmonary Disease

Abstract

Chronic obstructive pulmonary disease (COPD) and asthma are chronic inflammatory diseases of the airways. Galectin-13 has recently been forwarded as a biomarker for airway eosinophilic inflammation in asthma. However, the association between galectin-13 and COPD remains unknown. To examine the changes in galectin-13 expression in acute exacerbations of COPD (AECOPD) and the stable phase of COPD and unveil the association between galectin-13 expression and eosinophilic inflammation in COPD, we measured plasma galectin-13 expression in different phases of COPD patients (n = 60, 44 AECOPD patients, and 16 stable COPD patients) and healthy controls (n = 15). Plasma levels of galectin-13 in 60 COPD patients were further analyzed and compared to systemic inflammation, airway eosinophilic inflammation, and lung function. The plasma galectin-13 level was markedly increased in subjects with AECOPD compared to stable COPD patients and healthy controls. Plasma galectin-13 levels in COPD subjects were positively correlated with serum CRP (r_s = 0.46, p = 0.0003), peripheral blood eosinophilia count (r_s = 0.57, p<0.0001), and FeNO (r_s = 0.46, p = 0.0002). In addition, the level of galectin-13 was negatively correlated with FEV₁ (r_s = −0.43, p = 0.0001), FEV₁ pred (%) (r_s = −0.544, p<0.0001), as well as FEV₁/FVC (r_s = −0.46, p<0.0001). Multiple linear regression analysis suggested that plasma galectin-13 levels were affected by FEV₁ pred (%), peripheral blood eosinophilia count, and FeNO. We concluded that galectin-13 levels were increased in COPD patients, and elevated galectin-13 expressions related to airway eosinophilic inflammation. Galectin-13 may facilitate the identification of COPD endotypes and may become a potential therapeutic target.

Keywords:

• chronic obstructive pulmonary disease
• galectin-13
• eosinophilic inflammation
• CRP

Acknowledgements

We thank the patients who volunteered for this study.

Author contributions

L.Y. and S.Z. conceptualized the study design. L.Y., Y.F., D.C. and S.Z. collected demographic, clinical, and laboratory data. L.Y. and Y.J. analyzed the data. L.Y. and Y.J. interpreted the results. L.Y. and S.Z. wrote the manuscript with all authors providing feedback for revision. The authors read and approved the final report.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the National Natural Science Foundation of China (grants 81800026), the National Key Research and Development Program of China (2016YFC1304400).