COPD is a chronic inflammatory disease caused by inhalation of toxic particles and gases, mostly cigarette smoke (CS) [1–3,7]. Despite the fact that CS is the major risk factor for COPD, many chronic smokers maintain normal lung function (so-called resistant smokers) , so do some smokers even after more than 40 pack years of smoking , while only ~20–30% of chronic smokers develop the disease [1, 2,7,9]. This suggests that the susceptibility of smokers to COPD can vary significantly [1, 2, 8, 9]. However, the cellular and molecular basis for the disease susceptibility remains to be elucidated albeit genetic or environmental factors may play a role [1, 2]. As chronic cigarette smokers with normal lung function also have increased pulmonary inflammation, this inflammation seems to be magnified in COPD. Understanding of the amplification of inflammation is not yet complete . Cigarette smoking cessation is considered currently as the most important intervention to reduce COPD progression . While quitting smoking can prevent the COPD progression in some patients, who are referred as (reversibly) susceptible smokers, cigarette smoking cessation fails to slow or preclude the COPD progression in others (referred as severely susceptible smokers) [2, 11]. The precise understanding of different effects of smoking cessation has not yet been fully achieved [1–2].