Increased galectin-3 expression and intraepithelial neutrophils in small airways in severe chronic obstructive pulmonary disease

¹ Unit of Pneumology & Microbiology, University of Louvain
² Laboratory of Toxicology, Pharmacy School, Brussels, Belgium
³ Institute of Physiological Chemistry, Ludwig-Maximilians University, Munich, Germany
⁴ Laboratory of Histopathology, UCL Mont-Godinne, Belgium
⁵ Laboratory of Pneumology, University of Leuven, Leuven, Belgium

^* To whom correspondence should be addressed. E-mail: charles.pilette{at}pneu.ucl.ac.be.

	Abstract

Galectins-1 and -3 regulate epithelial proliferation/apoptosis and neutrophil activation, and are implicated in lung cancer and asthma. The role of galectins in chronic obstructive pulmonary disease (COPD), characterized by epithelial changes and neutrophil infiltration, remains unknown.

Galectin-1 and -3 expression was assessed by immunohistology in the bronchial epithelium of lung specimens from eight severe COPD patients, as compared to 9 nonsmokers and 6 smokers without COPD. Findings were related to epithelial proliferation (Ki-67), tissue inflammation and lung function.

Epithelial galectin-3 immunostaining was increased only in small airways of COPD as compared to nonsmokers (p<0.001) and smokers (p=0.002). In contrast, galectin-1 was significantly increased only in smokers' small airways (p<0.001). Ki-67+ epithelial cells were increased in COPD small airways as compared to smokers (p=0.05), as well as neutrophils. Moreover intraepithelial neutrophils correlated in small airways with Ki-67+ epithelial cells (p=0.03, r=0.76) and with the FEV₁/FVC ratio (p=0.001, K=-0.93), whereas no correlation was observed with galectin expression.

This study supports the hypothesis that distal airways represent an important site for detecting changes in COPD: in patients with severe disease we demonstrate increased galectin-3 expression and neutrophil accumulation in the small airway epithelium, correlating with epithelial proliferation and airway obstruction.

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