The effects of Ang-1, IL-8 and TGF-1β on the pathogenesis of COPD

Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent smoking-related disease for which no disease-altering therapies currently exist. Airway remodeling is one of the most important mechanisms in the pathogenesis of COPD and is triggered by chronic inflammation mediated by angiopoietin-1 (Ang-1), interleukin-8 (IL-8) and transforming growth factor-β1 (TGF-β1). The aim of this study was to investigate the effects of Ang-1, IL-8 and TGF-β1 on the pathogenesis of COPD. Forty-two COPD patients and 10 healthy adults (group A) were included in this study. We divided the 42 patients into 4 groups (groups B-E) according to the severity of the disease. We investigated the levels of Ang-1, IL-8 and TGF- β1 and the levels of pulmonary function (PF) in the stable and acute phases of COPD by enzyme-linked immunosorbent assay. We found statistically significant differences in the expression levels of Ang-1, IL-8 and TGF-β1 between the stable and acute phases in groups B-E. We found statistically significant differences in the expression levels of Ang-1 among all groups in the stable phase. In addition, there were statistically significant differences in the expression levels of TGF-β1 among all groups. There were statistically significant differences in the expression levels of IL-8 between group A and the other groups in the stable phase. Furthermore, in groups C-E we found higher correlations between Ang-1 and the forced expiratory volume in one second of forced vital capacity (FVC) [ FEV 1(%)] and FEV1/FVC(%) than between TGF-β1 and FEV1(%) and FEV1/FVC(%). We conclude that the blood vessel factor is more closely related to the pathogenesis of COPD.