title: Circulating levels of soluble Fas ligand in cachexic patients with COPD are higher than those in non-cachexic patients with COPD.
abstract: OBJECTIVE
  Apoptosis may be involved in the pathophysiology of cachexia in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study is to assess the potential role of the Fas-Fas ligand (FasL) system in cachexic patients with COPD.
  
  
  METHODS
  We measured the circulating levels of soluble FasL (sFasL), with a newly developed, highly sensitive enzyme-linked immunosorbent assay system in seventy patients with COPD and forty-seven control subjects.
  
  
  RESULTS
  The levels of sFasL in the COPD patients were significantly lower than those in the control subjects (46+/-29 vs. 55+/-28 pg/ml; p<0.05), whereas the levels of soluble Fas (sFas) remained unchanged between the two groups. The significant correlation between the levels of sFasL and sFas, observed in the control subjects (r=0.304; p<0.05), was absent in the COPD patients. Cachexic COPD patients with a relatively lower BMI (BMI <20 kg/m(2), n=45) and %fat (%fat <20%, n=34), showed significantly increased levels of sFasL compared to non-cachexic COPD patients with a relatively higher BMI (BMI > or =20 kg/m(2), n=25) and %fat (%fat > or =20%, n=36) (BMI; 51+/-33 vs. 36+/-15 pg/ml; p<0.05. %fat; 55+/-33 vs. 37+/-21 pg/ml; p<0.01), due to the inverse relationships between the body composition measurements and the levels of sFasL observed exclusively in the patients (BMI; r=-0.307; p<0.05. %fat; r=-0.283; p<0.05).
  
  
  CONCLUSIONS
  These results may suggest that the Fas-FasL system does not play a significant role in the potential triggers of enhanced apoptosis leading to skeletal muscle wasting and adipose tissue depletion in cachexic patients with COPD.
authors.affiliation: First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata.
authors.forename: Noriaki
authors.initials: N
authors.lastname: Takabatake
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Arao
authors.forename: Makoto
authors.initials: M
authors.lastname: Sata
authors.forename: Sumito
authors.initials: S
authors.lastname: Inoue
authors.forename: Shuichi
authors.initials: S
authors.lastname: Abe
authors.forename: Yoko
authors.initials: Y
authors.lastname: Shibata
authors.forename: Isao
authors.initials: I
authors.lastname: Kubota
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D000368:Aged; D017209:Apoptosis / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002100:Cachexia / Q000097:blood* / Q000209:etiology / Q000473:pathology; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D053222:Fas Ligand Protein; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000150:complications; D012720:Severity of Illness Index; D048069:Tumor Necrosis Factors / Q000097:blood*
chemical_list: D015415:Biomarkers; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D048069:Tumor Necrosis Factors