HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pilette, C. Articles by Sibille, Y. Search for Related Content PubMed PubMed Citation Articles by Pilette, C. Articles by Sibille, Y.

Increased galectin-3 expression and intra-epithelial neutrophils in small airways in severe COPD

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

CORRESPONDENCE: C. Pilette, Unit of Pneumology and Microbiology, University of Louvain, Avenue Hippocrate 54/5490, Brussels B-1200, Belgium. Fax: 32 7649440. E-mail: charles.pilette{at}pneu.ucl.ac.be

Keywords: Epithelial proliferation, galectin, hyperplasia, inflammation, lung

Received: June 25, 2005
Accepted January 3, 2007

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), characterised by epithelial changes and neutrophil infiltration, remains unknown.

In the present study, galectin-1 and -3 expression was assessed by immunohistology in the bronchial epithelium of lung specimens from eight severe COPD patients and compared with nine nonsmokers and six smokers without COPD. Findings were related to epithelial proliferation (Ki-67), tissue inflammation and lung function.

Epithelial galectin-3 immunostaining was increased only in the small airways of COPD patients when compared with nonsmokers and smokers. In contrast, galectin-1 was only significantly increased in the small airways of the group of smokers. Ki-67+ epithelial cells and neutrophils were increased in the small airways of COPD patients when compared with smokers. Furthermore, intra-epithelial neutrophils correlated in the small airways with Ki-67+ epithelial cells and with the forced expiratory volume in one second/forced vital capacity ratio. However, no correlation was observed with galectin expression.

The present study supports the hypothesis that distal airways represent an important site for detecting changes in chronic obstructive pulmonary disease. In patients with severe disease, an increased galectin-3 expression and neutrophil accumulation in the small airway epithelium was demonstrated, correlating with epithelial proliferation and airway obstruction.