title: Circulating levels of soluble Fas ligand and soluble Fas in patients with chronic obstructive pulmonary disease.
abstract: Fas- and tumour necrosis factor (TNF) receptor-mediated apoptosis are known to be two principal apoptotic mechanisms in humans. Although there are several distinctions between these two systems, in vitro studies have demonstrated similar hypoxic activation and a functional relationship. Since patients with chronic obstructive pulmonary disease (COPD) show chronic hypoxaemia and the activation of the TNF-alpha system, we investigated whether these pathophysiological changes influence the Fas-Fas ligand system. We measured the circulating soluble Fas ligand (sFas-L) level, an inducer of apoptosis, and the soluble Fas receptor (sFas) level, an inhibitor of apoptosis, in 34 COPD patients and 35 age-matched healthy controls. In addition, we investigated the relationships between the levels of sFas-L or sFas and clinical variables including the TNF-alpha system; circulating TNF-alpha and soluble TNF-receptor (sTNF-Rs: sTNF-R55 and R75) levels, in the COPD patients. Although circulating TNF-alpha, sTNF-R55 and R75 levels were significantly higher in the COPD patients than in the healthy controls, serum level of sFas-L (Fisher's exact probability test; P = 0.26) and plasma level of sFas [COPD patients vs. controls; mean (SD); 3.74 (0.63) vs. 3.67 (0.48) ng/ml; P = 0.89) were not increased in the COPD patients. There was no significant correlation between the levels of sFas-L or sFas and clinical variables in COPD patients. These results suggest that the Fas-Fas ligand system does not independently play an important role in the pathophysiology of patients with COPD.
authors.affiliation: First Department of Internal Medicine, Yamagata University School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Takabatake
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
authors.forename: S
authors.initials: S
authors.lastname: Inoue
authors.forename: K
authors.initials: K
authors.lastname: Terashita
authors.forename: H
authors.initials: H
authors.lastname: Yuki
authors.forename: S
authors.initials: S
authors.lastname: Kato
authors.forename: S
authors.initials: S
authors.lastname: Yasumura
authors.forename: H
authors.initials: H
authors.lastname: Tomoike
mesh_terms: D000368:Aged; D001784:Blood Gas Analysis; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000097:blood* / Q000503:physiopathology; D008297:Male; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D013147:Spirometry; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019014:fas Receptor / Q000097:blood*
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor