The Pathology of Chronic Obstructive Pulmonary Disease

被引:541
|
作者
Hogg, James C. [1 ,2 ]
Timens, Wim [3 ]
机构
[1] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V6Z 1Y6, Canada
[2] St Pauls Hosp, iCapture Ctr, Vancouver, BC V6Z 1Y6, Canada
[3] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol, NL-9700 RB Groningen, Netherlands
基金
加拿大健康研究院;
关键词
emphysema; remodeling; smoking; tissue repair; CHEMOKINE RECEPTOR CXCR3; AIRWAY EPITHELIAL-CELLS; LYMPHOID-TISSUE BALT; HUMAN BONE-MARROW; CIGARETTE-SMOKE; CHRONIC-BRONCHITIS; PERIPHERAL AIRWAYS; LUNG-DISEASE; ALVEOLAR MACROPHAGES; LEUKOCYTE COUNT;
D O I
10.1146/annurev.pathol.4.110807.092145
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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.
引用
收藏
页码:435 / 459
页数:25
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