Circulating Levels of Soluble Fas Ligand in Cachexic Patients with COPD are higher than those in Non-Cachexic Patients with COPD

Abstract

ObjectiveApoptosis 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.Patients and 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 20 kg/m 2 , n=25) and %fat (%fat 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).Conclusion These results may suggest that the FasFasL 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. (Internal Medicine 44: 1137-1143, 2005)

Identification of key genes and biological pathways in chronic obstructive pulmonary disease using bioinformatics and next generation sequencing data analysis

“…Signaling pathways include immune system [109], signal transduction [110], extracellular matrix organization [111], adaptive immune system [112], neutrophil degranulation [113], innate immune system [114], metabolism [115], diseases of metabolism [116] and Hemostasis [117] were responsible for advancement of COPD. PTGS2 [118], IL6 [119], CSF3 [120], CXCL8 [121], CXCL1 [122], SOCS3 [123], CCL3 [124], CCL5 [125], VCAM1 [126], CXCL13 [127], CXCL5 [128], CXCL12 [129], FGG (fibrinogen gamma chain) [130], IL1B [131], AREG (amphiregulin) [132], SERPINE1 [133], OSM (oncostatin M) [134], CCL11 [135], MFAP4 [136], APLN (apelin) [137], IL1RN [138], IFNG (interferon gamma) [139], CX3CL1 [140], CDKN1A [141], ICAM1 [142], SNAI1 [143], CD34 [144], IL33 [145], FASLG (Fas ligand) [146], FGF7 [147], TNF (tumor necrosis factor) [148], GDF15 [149], CCL22 [150], IL2 [151], CXCR6 [152], KLF5 [153], MCL1 [154], SRF (serum response factor) [155], FABP4 [156], CYP2C19 [157], CXCR4 [158], FOXC1 [159], EPHX1 [160], ANXA1 [161], DUSP6 [162], CPA3 [163], MYH10 [164], ICOS (inducible T cell costimulator) [165], CD1C [166], CD96 [167], S100A9 [168], FKBP5 [169], HMOX1 [170], PRTN3 [171], MARCO (macrophage receptor with collagenous structure) [172], STAB1 [173], SIGLEC9 [174], SLC11A1 [175], BPI (bactericidal permeability increasing protein) [176], PGF (placental growth factor) [177], FASN (fatty acid synthase) [178], S100A4 […”