ABSTRACT
Chronic obstructive pulmonary disease (COPD) is global health problem with
increasing morbidity and mortality (1). COPD is characterized by airflow
limitation that is not fully reversible, usually progressive, and associated with an
abnormal inflammatory response of the lungs following exposure to noxious
particles and gases and inhaled cigarette smoke (2,3). One important pathological
feature of COPD is airway inflammation, characterized by an influx of
neutrophils, macrophages, and CD8CT-lymphocytes in the lumen and wall of
bronchial and bronchiolar airways and parenchyma (4-6). Over time, alveolar
destruction results in emphysema, and chronic bronchial inflammation leads to
chronic bronchitis-which is why COPD is often called “emphysema and
chronic bronchitis” (7). Interestingly, only 10% to 20% of all smokers develop
symptomatic COPD; yet the causes of this variability in response of the airways
and lung parenchyma to tobacco smoke exposure remain largely unclear.
