• J C Hogg.
• University of British Columbia, McDonald Research Laboratories, St Paul's Hospital, Vancouver, British Columbia, Canada. jhogg@mrl.ubc.ca
• Int. J. Tuberc. Lung Dis. 2008 May 1; 12 (5): 467-79.

AbstractThe pathogenesis of chronic obstructive pulmonary disease (COPD) is related to a chronic innate and adaptive inflammatory immune response to inhaled toxic particles and gases, primarily as a result of the tobacco smoking habit. This inflammatory immune process develops in the lungs of everyone that smokes, and there is an association between the extent and severity of this tissue response and the severity of airflow limitation present in the fraction of the smoking population that develops COPD. This infiltration of inflammatory immune cells into the lung tissue is inextricably linked to a tissue repair and remodeling process that enlarges the bronchial mucus glands, thickens the walls and narrows the lumen of conducting airways <2 mm in diameter. A multivariate analysis has shown that thickening of the walls of the small conducting airways and occlusion of their lumen by inflammatory exudates containing mucus explains more of the variance in the association between FEV1 decline and histology in COPD than the infiltration of the tissue by any inflammatory cell type. Emphysematous destruction of the gas exchanging tissue also contributes to the airflow limitation by reducing the elastic recoil pressure available to drive air out of the lung during forced expiration. This tissue destruction begins in the respiratory bronchioles in very close proximity to the small conducting airways that become the major site of obstruction in COPD. The mechanism(s) that allow small airways to thicken in such close proximity to lung tissue undergoing emphysematous destruction remain a puzzle that needs to be solved. As the accumulation of tissue responsible for thickening the small conducting airways is a very different pathological process from the emphysematous destruction of surrounding gas exchanging tissue, we need a better understanding of the pathogenesis of both processes and better methods of separating their relative contribution to airflow limitation in individuals to adequately prevent and treat COPD.

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