-
- James C. Hogg
- Department of Pathology and Laboratory Medicine, University of British Columbia and iCapture Center, St. Paul's Hospital, Vancouver, British Columbia V6Z 1Y6, Canada;
-
- Wim Timens
- Department of Pathology, University Medical Center Groningen, University of Groningen, Groningen 9700 RB, The Netherlands;
抄録
<jats:p> The pathogenesis of chronic obstructive pulmonary disease (COPD) is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although tobacco smoking is the primary cause of this inhalation injury, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue-repair and -remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The common form of emphysema observed in smokers begins in the respiratory bronchioles near the thickened and narrowed small bronchioles 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 remains a puzzle that needs to be solved. </jats:p>
収録刊行物
-
- Annual Review of Pathology: Mechanisms of Disease
-
Annual Review of Pathology: Mechanisms of Disease 4 (1), 435-459, 2009-02-01
Annual Reviews