Transcript levels of COX-2, TNF-α, IL-6 and IL-10 in chronic obstructive pulmonary disease: An association with smoking and severity

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by inflammation. Tobacco smoking plays an important role in inflammation and subsequent disease progression. Therefore, inflammatory biomarkers (COX-2, TNF-α, IL-6 and IL-10 genes) expression levels were marked in patients with and without smoking habits and the severity of COPD. The severity of COPD, spirometry results and pack-years of smoking were assessed. The mRNA levels of COX-2, TNF-α, IL-6 and IL-10 in peripheral blood mononuclear cells were evaluated using reverse transcriptase-polymerase chain reaction. Relative fold expression and Pearson correlations were established among the group variables. Patients had a higher expression of COX-2 followed by TNF-α and IL-6 (p<0.000). In contrast, IL-10 expression was decreased by half in patients compared to controls (p<0.0001). COX-2 (10.37-fold), IL-6 (11.31-fold) and TNF-α (6.86-fold) were highly expressed in smokers (P <0.0001). In contrast, IL-10 expression was dramatically lower in smokers than non-smokers (p<0.0001). With increasing smoking pack-years, COX-2, TNF-α and IL-6 expression were significantly increased, but IL-10 gene expression was decreased (p<0.05). COX-2, TNF-α and IL-6 gene expression progressively increased with severity grade, but IL-10 expression was dramatically reduced (p<0.0001). COX-2 was positively correlated with TNF-α and IL-6 (r=0.39, p<0.0001) whereas COX-2 was moderately correlated with IL-10 (r=-0.62 and 0.63, p<0.0001). The higher expression of COX-2, TNF-α and IL-6 in patients with COPD suggests that these patients will likely benefit from COX-2, TNF-α and IL-6 blockers. Smoking cessation reduces the burden and severity of COPD.