The CS-induced inflammatory response in COPD progression involving both innate and adaptive immunity [1, 2] is mediated via a complex network that encompasses multiple immune cell types, molecular mediators and lung tissues. Several different types of immune cells and molecular mediators are found to accumulate in the lungs of patients with COPD [1–3, 5–7, 12]. Important immune cells include macrophages, neutrophils, dentritic cells, and T lymphocytes and molecular mediators include cytokines, chemokines, and protein proteases such as metalloproteases (MMPs). There exists an enormous amount of literature regarding these individual network elements. However, little is known about combined interactions between these elements or the associated pathways in the network. In particular, while COPD progression is a multistage and dynamic process, studies on the temporal sequence of inflammation in the disease are lacking . It is not clear how immune cells and molecular mediators are dynamically linked and which of these elements are determinants in the disease progression. This is particularly important for identification of biomarkers in the disease [6, 13–17]. For example, the levels of proinflammatory cytokines, TNF-α and IL-1β are increased in the lungs of COPD patients and were suggested as potential targets . However, inhibition of TNF-α or IL-1β has been proved to be unsuccessful in clinical trials of patients with COPD . A pilot study on patients with COPD revealed no change in levels of inflammatory markers following inhibition of TNF-α , but the underlying reason remains to be elucidated [6, 19]. Recent studies have shown that the levels of IL-6 as well as the associated proteins, C-reactive protein (CRP) and fibrinogen, are significantly increased in COPD patients compared to those in smokers with normal lung function and healthy non-smokers . IL-6 is considered to be a potential biomarker for COPD, but the detailed mechanism of IL-6 action in the disease progression is not yet fully understood.