An increase of soluble Fas, an inhibitor of apoptosis, associated with progression of COPD

In chronic obstructive pulmonary disease (COPD) which consists of emphysema and chronic bronchitis, alveolar tissue and/or bronchiolar walls are progressively destroyed.This suggests cell death by necrosis and/or apoptosis although no direct evidence of apoptosis has been reported.It was speculated that the apoptosis-related factors are associated with the progression of COPD.Fas/Apo-1 receptor (Fas), Fas ligand (Fas-L) and soluble Fas ligand (sFas-L) are inducers, while soluble Fas (sFas) is an inhibitor of apoptosis.In this study, plasma sFas and sFas-L were measured in 19 COPD patients receiving supplemental 0, (severe COPD) and 20 COPD patients not receiving supplemental 0, (mild/moderate COPD).Twenty-two age-and sex-matched healthy volunteers (healthy controls) and 20 patients receiving supplemental 0, and with levels of hypoxaemia similar to severe COPD due to other pulmonary diseases (disease controls) were also examined.Plasma sFas-L was within normal limits in all groups.Plasma sFas levels were similar among healthy controls, disease controls, and mild/moderate COPD patients, but significantly increased in severe COPD (2.6 l 1.1, 2.6 i 0.2, 2.8 & 0.2 and 4.8 * 1 .O ng ml -', respectively).Although PaO, was lower in severe COPD than in mild/moderate COPD, and PaCO, was higher in severe COPD than in mild/moderate COPD, they were close between severe COPD and disease controls.Tumour necrosis factor-a (TNF-a), interleukin 6 (IL-6) and C-reactive protein (CRP) were increased in patients with COPD, but were similar in both severe and mild/moderate COPD patients.We conclude that increased plasma sFas, which is independent of hypoxaemia, and increases in PaCO,, TNF-a, IL-6 and inflammation, may be associated with progression of COPD.