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

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-alpha, 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-alpha, 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-alpha 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-alpha (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-alpha and IL-6 expression were significantly increased, but IL-10 gene expression was decreased (p<0.05). COX-2, TNF-alpha 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-alpha 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-alpha and IL-6 in patients with COPD suggests that these patients will likely benefit from COX-2, TNF-alpha and IL-6 blockers. Smoking cessation reduces the burden and severity of COPD.