Circulating levels of soluble Fas ligand and soluble Fas in patients with chronic obstructive pulmonary disease

Fas- and tumour necrosis factor (TNF) receptor-mediated apoptosis are known to be two principal apoptotic mechanisms in humans. Although there are sev eral distinctions between these two systems, in vitro studies have demonstr ated similar hypoxic activation and a functional relationship. Since patien ts with chronic obstructive pulmonary disease (COPD) show chronic hypoxaemi a and the activation of the TNF-alpha system, we investigated whether these pathophysiological changes influence the Fas-Fas ligand system. We measure d the circulating soluble Fas ligand (sFas-L) level, an inducer of apoptosi s, and the soluble Fas receptor (sFas) level, an inhibitor of apoptosis, in 34 COPD patients and 35 age-matched healthy controls. In addition, we inve stigated the relationships between the levels of sFas-L or sFas and clinica l variables including the TNF-alpha system; circulating TNF-alpha and solub le TNF-receptor (sTNF-Rs: sTNF-R55 and R75) levels, in the COPD patients. A lthough circulating TNF-alpha, sTNF-R55 and R75 levels were significantly h igher in the COPD patients than in the healthy controls, serum level of sFa s-L (Fisher's exact probability test; P=0.26) and plasma level of sFas [COP D patients rs. controls; mean (SD); 3.74 (0.63) vs. 3.67 (0.48)ng/ml; P=0.8 9) were not increased in the COPD patients. There was no significant correl ation between the levels of sFas-L or sFas and clinical variables in COPD p atients. These results suggest that the Fas-Fas ligand system does not inde pendently play an important role in the pathophysiology of patients with CO PD.