Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitations, that are not fully reversible. COPD is a major cause of chronic morbidity and mortality throughout the world. Tobacco smoking is a most important risk factor for the development of COPD. However, only 10 to 20% smokers develop clinically significant COPD. The detailed pathogenesis also remains to be elucidated. In vivo animal models provided some clues to help clarify the pathogenesis. Several important factors such as matrix metalloproteinases, apoptosis, protease-antiprotease imbalance, are considered to contribute to the development of COPD. In addition to these factors, chronic inflammation affects lung morphogenesis and causes several pathological involvements including COPD. In this article, we review the pathogenesis of COPD, while especially focusing on the recent advances and the effects of chronic inflammation using an in vivo animal model. This article aims at offering valuable information for both proceeding with COPD research as well as for developing a new medicines for the treatment of COPD.

Keywords: Air Pollutants - toxicity, Gene Targeting, Inflammation - etiology, Matrix Metalloproteinases - physiology, Pancreatic Elastase - physiology, Pulmonary Disease, Chronic Obstructive - physiopathology, Risk Factors, Smoking - adverse effects