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Acta Medica Medianae
Vol. 45
Number 1, Januar, 2006
UDK 61
YU ISSN 0365-4478


Miloš Filipović
Pulmonary Clinic
Dr Zoran Djindjic Street
18000 Nis, Serbia and Montenegro
Tel.:018/ 233-355
E-mail: milosfilip@yahoo.com



Copyright 2006 by Faculty  of Medicine, University of Nis


 Milos Filipovic 1, Boris Djindjic 2 and Snezana Cekic 3

Pulmonary Clinic of Nis1
Institute of Pathofiziology of the Faculty of Medicine of Ni

Institute of Fiziology of the
Faculty of Medicine of Nis3

 Chronic obstructive pulmonary disease (COPD) is an obstructive pulmonary disorder which is characterized by limitation of expiratory airflow that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. The inflammatory process associated with COPD is characterized by increased number of activated alveolar macrophages, neutrophils, CD8+ cytotoxic T lymphocytes, B lymphocytes and CD4+ T lymphocytes, and the release of numerous inflammatory mediators (leukotrienes, cytokines, growth factors, chemokines, oxidants and proteases). Chronic inflammation causes remodeling of the small airways with the luminal obstruction due to increased mucus production and thickened walls due to edema and collagen formation that cause fibrosis and narrowing of small airways. Persistent inflammation also leads to destruction of lung tissue, loss of alveolar attachment to the small airways, and decreased lung elastic recoil. Although COPD affects the lungs, it also produces significant systemic consequences. Acta Medica Medianae 2006:45(1):73–81.

Key words: bronchitis, emphysema, cigarette smoking, protease, matrix metalloproteinases, oxidative stress, alveolar macrophage, neutrophil, cytokine, mucociliary