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Accessible online at: www.karger.com/res Chronic obstructive pulmonary disease (COPD) is characterized by structural changes in the central and peripheral airways producing irreversible, progressive obstruction of expiratory flow [1]. The pathological changes characteristic of COPD include inflammation of the large and small airways, enlarged mucus secreting glands with an increased number of goblet cells and mucus hypersecretion, structural remodeling of the airway wall, with increased collagen content and scar tissue formation, and, finally, dilatation and destruction of the respiratory bronchioles [1]. Recent studies have greatly improved our understanding of the pathogenetic mechanisms underlying COPD [1, 2]. Indeed, it has been demonstrated that persistent airway inflammation is characterized not only by high numbers of neutrophils but also by the presence of activated macrophages and T-lymphocytes (predominant CD8+) [1–3]. These immunoeffector cells release a variety of mediators, including leukotriene B4 (LTB4), interleukin-8 (IL-8), and tumour necrosis factor-· (TNF-·), capable of sustaining the neutrophilic inflammation that characterizes the disease [3, 4]. The recruitment and activation of neutrophils lead to the production of large amounts of toxic oxygen radicals and to the release of granule-associated preformed enzymes [2, 4]. The resulting oxidative stress and proteinase-antiproteinase imbalance is a key factor in inducing the chronic injury to the lung parenchymal cells and the destruction of the airway structures described in COPD patients [1, 2]. The inflammatory process within the lungs is thought to be caused and maintained by environmental exposure to inhaled noxious particles and gases in subjects genetically predisposed to develop the disease. Although occupational dusts and chemicals and outdoor and indoor air pollutants may play a relevant role, cigarette smoking is considered the major factor involved in the pathogenesis of COPD [2]. Indeed, cigarette smoke can not only induce activation of inflammatory mechanisms and directly damage the lungs but also adversely affect the repair mechanisms activated in response to this injury. Insufficient repair of alveolar structures leads to emphysema with destruction of alveolar attachments, while repair with scarring is likely to lead to irreversible and progressive airflow limitation [1, 2]. Active smokers have a higher prevalence of lung function abnormalities and respiratory symptoms, a greater annual rate of decline in FEV1, and higher death rates for COPD than nonsmokers [5], but also passive exposure to cigarette smoke, increasing lung total burden of inhaled particulates and gases, may contribute to respiratory structure injury [6].

COPD Patients or ‘Healthy Smokers’: Is IL-8 Synthesis and Release the Borderline?