Endothelial interactions of neutrophils under flow in chronic obstructive pulmonary disease
IS Woolhouse, DL Bayley, P Lalor… - European …, 2005 - Eur Respiratory Soc
European Respiratory Journal, 2005•Eur Respiratory Soc
It is generally accepted that the neutrophil is central to the pathogenesis of chronic
obstructive pulmonary disease (COPD). Enhanced endothelial interactions of this cell may
contribute to the susceptibility of smokers who develop the disease; however, these
interactions have not previously been studied in COPD. The aim of the current study was to
determine whether enhanced endothelial interactions of neutrophils from smokers are a
predisposing factor for the development of COPD. Endothelial interactions under flow and …
obstructive pulmonary disease (COPD). Enhanced endothelial interactions of this cell may
contribute to the susceptibility of smokers who develop the disease; however, these
interactions have not previously been studied in COPD. The aim of the current study was to
determine whether enhanced endothelial interactions of neutrophils from smokers are a
predisposing factor for the development of COPD. Endothelial interactions under flow and …
It is generally accepted that the neutrophil is central to the pathogenesis of chronic obstructive pulmonary disease (COPD). Enhanced endothelial interactions of this cell may contribute to the susceptibility of smokers who develop the disease; however, these interactions have not previously been studied in COPD. The aim of the current study was to determine whether enhanced endothelial interactions of neutrophils from smokers are a predisposing factor for the development of COPD.
Endothelial interactions under flow and adhesion molecule expression of peripheral blood neutrophils were compared between seven never-smokers (NS), seven healthy smokers (HS), 11 COPD patients with severe α1-antitrypsin deficiency (PiZ) and neutrophils from 11 COPD patients without the deficiency (PiM).
Total adhesive and migratory responses (per mm2 endothelium per 106 neutrophils) were significantly greater in the PiM group (mean±se 704.2±57.9 versus 509.3±48.8 in the PiZ group, 499.3±40.1 in the HS and 491.2±33.7 in the NS). This corresponded with increased macrophage antigen-1 (CD11b) expression on stimulated neutrophils in the PiM group compared with the PiZ group (mean±se relative fluorescence intensity 1.4±0.1 versus 1.1±0.1).
In conclusion, the enhanced endothelial interaction of neutrophils from smokers who have developed chronic obstructive pulmonary disease in the presence of normal levels of α1-antitrypsin deficiency, but not in those with severe α1-antitrypsin deficiency, suggests that this is a predisposing factor for the development of the disease, and upregulation of macrophage antigen-1 may be responsible.
European Respiratory Society