oa Editorial [Hot Topic: Chronic Obstructive Pulmonary Disease (COPD) (Guest Editor: Alexandre Trifilieff)]

Chronic obstructive pulmonary disease (COPD) is a multi-component disease (including emphysema and chronic bronchitis which may or may not co-exist in the same individual) leading to a disease state characterized by poorly reversible airflow limitation that is usually progressive and associated with an abnormal inflammatory response of the lung. This disease constitute a major public health burden worldwide and the World Health Organization estimates COPD to be the world's fifth most common disease and fourth leading cause of death [1]. Both prevalence and mortality are expected to increase in the coming decades. Cigarette smoking is the major risk factor for development of COPD, and smoking cessation is the only intervention that slows the disease progression. Very few effective therapies are available and bronchodilatator therapy, such as long acting inhaled β2 agonists or inhaled anticholinergic agents, is the mainstay of the management of this disease. For comprehensive reviews about the current management of COPD the reader can refer to two recently published reviews [2, 3]. The pathophysiology of COPD is multifactorial with an inflammatory cells profile that includes macrophages, neutrophils and T lymphocytes. However, the precise mechanism leading to this lung inflammation is still unclear and currently no pharmacological intervention has been shown to modify the progression of the disease or the associated decline in health status. Although this disease was neglected in the past, recently an increased number of studies have been trying to define more precisely the mechanism underlying this pathology. Consequently, our understanding of this disease has recently improved and this dedicated issue is aiming at cover the latest developments in this topic. The inflammatory process is covered by T. D. Tetley with a focus on the inflammatory cell types involved in this disease and K. F. Chung who recapitulated the various inflammatory mediators that could be involved. W. MacNee has reviewed the oxidant/anti-oxidant imbalance hypothesis in this disease. W. Davidson and T. R. Bai, summarized the lung structural changes associated with this pathology and H. Danahay and A. D. Jackson put forward hypotheses that could help to determine the mechanisms behind epithelial dysfunction in respiratory diseases. R. Mahadeva and S. D. Shapiro have described the pro and con of the animal models of pulmonary emphysema. Finally, P. J. Barnes has put together a list of emerging targets that could well be the future treatments for this disease. I would like to express my gratitude to all the contributors and hope the reader will benefit from reading this special issue on COPD. REFERENCES [1] Murray, C.J.; Lopez, A.D. Science, 1996, 274, 740. [2] Wouters, E.F. Lancet, 2004, 364, 883. [3] Sutherland, E.R.; Cherniack, R.M. N. Engl. J. Med., 2004, 350, 2689.