1. The Pathology of Chronic Obstructive Pulmonary Disease
- Author
-
James C. Hogg and Wim Timens
- Subjects
LUNG-DISEASE ,Male ,Chronic bronchitis ,Pathology ,medicine.medical_specialty ,Pyridines ,Hypertension, Pulmonary ,CHEMOKINE RECEPTOR CXCR3 ,PERIPHERAL AIRWAYS ,smoking ,Pathology and Forensic Medicine ,Pathogenesis ,Pulmonary Disease, Chronic Obstructive ,Risk Factors ,Animals ,Humans ,Medicine ,tissue repair ,Pulmonary pathology ,ALVEOLAR MACROPHAGES ,Lung ,remodeling ,Aged ,Asthma ,COPD ,Inhalation ,business.industry ,LYMPHOID-TISSUE BALT ,Middle Aged ,medicine.disease ,Pulmonary hypertension ,AIRWAY EPITHELIAL-CELLS ,Immunity, Innate ,Hydroquinones ,respiratory tract diseases ,emphysema ,CHRONIC-BRONCHITIS ,LEUKOCYTE COUNT ,medicine.anatomical_structure ,Pulmonary Emphysema ,CIGARETTE-SMOKE ,Immunology ,Female ,Pulmonary Ventilation ,business ,HUMAN BONE-MARROW - Abstract
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.
- Published
- 2009
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