MicroRNA-218 acts by repressing TNFR1-mediated activation of NF-κB, which is involved in MUC5AC hyper-production and inflammation in smoking-induced bronchiolitis of COPD.

Dysregulation of microRNAs (miRNAs) has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is largely attributable to cigarette smoke (CS). However, little is known about the effect of miRNAs on CS-induced mucus hypersecretion and the inflammatory response in the airway epithelium, which are pathological characteristics of COPD-related chronic bronchiolitis. As determined in the present investigation, population-based data indicate that smokers with COPD had serious airflow obstruction and inflammation, whereas smokers without COPD had mild airflow obstruction and inflammation. Moreover, levels of serum miR-218 positively correlated with FEV