title: An increase of soluble Fas, an inhibitor of apoptosis, associated with progression of COPD.
abstract: 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 O2 (severe COPD) and 20 COPD patients not receiving supplemental O2 (mild/moderate COPD). Twenty-two age- and sex-matched healthy volunteers (healthy controls) and 20 patients receiving supplemental O2 and with level 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 +/- 1.1, 2.6 +/- 0.2, 2.8 +/- 0.2 and 4.8 +/- 1.0 ng ml-1, respectively). Although PaO2 was lower in severe COPD than in mild/moderate COPD, and PaCO2 was higher in severe COPD than in mild/moderate COPD, they were close between severe COPD and disease controls. Tumour necrosis factor-alpha (TNF-alpha), 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 PaCO2, TNF-alpha, IL-6 and inflammation, may be associated with progression of COPD.
authors.affiliation: Second Department of Internal Medicine, Gifu University School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Yasuda
authors.forename: K
authors.initials: K
authors.lastname: Gotoh
authors.forename: S
authors.initials: S
authors.lastname: Minatoguchi
authors.forename: K
authors.initials: K
authors.lastname: Asano
authors.forename: K
authors.initials: K
authors.lastname: Nishigaki
authors.forename: M
authors.initials: M
authors.lastname: Nomura
authors.forename: A
authors.initials: A
authors.lastname: Ohno
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: H
authors.initials: H
authors.lastname: Kumada
authors.forename: T
authors.initials: T
authors.lastname: Sawa
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D002245:Carbon Dioxide / Q000097:blood; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008173:Lung Diseases, Obstructive / Q000097:blood* / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019014:fas Receptor / Q000097:blood*
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D002245:Carbon Dioxide; D010100:Oxygen