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Chronic obstructive pulmonary disease (COPD) is characterised by a chronic inflammation in the pulmonary tissue. The disease is associated with a switch from a self-limiting inflammatory response, mainly initiated by smoke inhalation, to a chronic persistent inflammatory response after prolonged interaction with cigarette smoke. The development and progression of chronic obstructive pulmonary disease have been associated with increased oxidative stress and reduced antioxidant resources. As a result, the antioxidant capacity decreases in COPD patients. Additionally, there is an imbalance between the release of proteases and of endogenous anti-protease enzymes that prevent elastin digestion. The inflammatory basis of COPD is now well established. In patients with COPD increased numbers of macrophages and neutrophils have been found in induced sputum, the former predominating in mild disease. Biopsy data confirm these observations but also demonstrate increased numbers of CD8-positive T- lymphocytes in the airway wall, which may have a role in the regulation of the inflammatory response to cigarette smoke. The extent of the inflammatory reaction is correlated with the severity of the disease. An imbalance between pro- and anti-inflammatory cytokines may favour this process. Several mediators are involved in COPD including leukotriene B4 (LTB4), tumor necrosis factor alpha (TNF-alpha), and interleukin8 (IL-8). They are selective attractants of neutrophils and regulate the ongoing inflammatory process. The whole process would be predicted to be self-perpetuating leading to a chronic inflammatory state with associated airway remodelling and progressive lung function decline.

The healing process of skin wounds is regulated by growth factors which stimulate proliferation of resident cells and their synthesis of extra cellular matrixcomponents. Different leukocyte subtypes (neutrophils, macrophages, lymphocytes and mast cells) participate in wound healing not only as immunological effector cells but also as an important source of inflammatory and growth promoting cytokines. Rapid recruitment of leukocytes and their positioning is tightly regulated by a temporally and spatially changing set of chemokines. Whereas expression of IL-8 and GRO (growth related oncogene) direct early neutrophil recruitment, migration of macrophages is stimulated by MCP-1 (monocyte chemoattractant protein-1) and later, lymphocytes are attracted by IP-10 (gamma-interferon inducible protein-10) and Mig (monokine induced by interferon-gamma). Since chemokines as IL-8 and GRO also stimulate angiogenesis and keratinocyte proliferation, they integrate the inflammatory events with the reparative processes and are potential candidates in the search of wound healing agents.