Smoking is the main etiologic factor in chronic obstructive pulmonary disease (COPD). Cigarette smoke produces an enormous oxidant burden on the lungs, which is exacerbated by the release of oxidants from inflammatory cells. There is considerable evidence that an increased oxidative burden occurs in the lungs of patients with COPD, and this may be involved in many of the pathogenic processes, such as direct injury to lung cells, mucus hypersecretion, inactivation of antiproteases, and enhancing lung inflammation through activation of redox-sensitive transcription factors. COPD is also recognized to have multiple systemic consequences, such as weight loss and skeletal muscle dysfunction. Moreover, it is appreciated that oxidative stress extends beyond the lung and may, through similar oxidative stress mechanisms as those in the lung, contribute to several of the systemic manifestations in COPD such as skeletal muscle dysfunction. Thus, there is a great need for an effective antioxidant therapy to modulate the oxidative stress in COPD, since this may be an important therapeutic target.
Keywords: inflammatory cells, Cigarette smoke, alveolar macrophages, Oxidative Stress, protease burden, mucus secretion
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