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Chronic obstructive pulmonary disease (COPD) is a prevalent smoking-relateddisease for which no disease‑altering therapies currently exist. Airway remodelingis one of the most important mechanisms in the pathogenesis of COPD and is triggeredby 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 investigatethe effects of Ang-1, IL-8 and TGF-β1 on the pathogenesis of COPD. Forty-two COPDpatients and 10 healthy adults (group A) were included in this study. We dividedthe 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 pulmonaryfunction (PF) in the stable and acute phases of COPD by enzyme-linked immunosorbentassay. We found statistically significant differences in the expression levelsof Ang-1, IL-8 and TGF-β1 between the stable and acute phases in groups B-E. Wefound statistically significant differences in the expression levels of Ang-1among all groups in the stable phase. In addition, there were statistically significantdifferences in the expression levels of TGF-β1 among all groups. There were statisticallysignificant differences in the expression levels of IL-8 between group A and theother groups in the stable phase. Furthermore, in groups C-E we found higher correlationsbetween 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 pathogenesisof COPD.

The effects of Ang-1, IL-8 and TGF-β1 on the pathogenesis of COPD