ABSTRACT
Chronic obstructive pulmonary disease (COPD) is amongst the commonest diseases in the world, with an alarming increase in global prevalence [1]. Cigarette smoking is the major risk factor for the development of COPD and cigarette smokers constitute over 90% of COPD patients in developed countries. The incidence of COPD is rising worldwide and there is a need to develop new treatments to prevent the progression of the disease, which results in a large consumption of health care resources [2]. COPD involves fixed airflow limitation and chronic inflammation of the lower airways and is characterised by the expression of multiple inflammatory proteins, including cytokines, chemokines, adhesion molecules, enzymes producing inflammatory mediators and inflammatory mediator receptors [2,3]. Most of these proteins are regulated at the transcriptional level, suggesting that in both diseases transcription factors may play an important role [4,5]. Nuclear factor-kappaB (NF-κB) regulates many of the genes that are abnormally expressed in COPD and is activated in the lower airways of patients with COPD [6]. One clear difference between COPD and other chronic inflammatory diseases of the lower airways such as asthma is the clinical responsiveness to corticosteroids.
