The effects of Ang-1, IL-8 and TGF-β1 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 (groupA) were included in this study. We divided the 42 patients into 4 groups (groupsB-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) [FEV1(%)] 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.