Chronic Obstructive Pulmonary Disease (COPD) is an obstructive airways
disease, characterised by a
partially reversible, but progressive worsening obstruction of airflow. COPD is
an umbrella term which encompasses pulmonary emphysema and chronic bronchitis1. It is well-known that cigarette smoking is
the key risk-factor for an individual developing COPD. Despite the fact that
all cigarette smokers evoke a degree of inflammation and subsequently damage to
the airway epithelium, the number of individuals who consequentially develop
COPD remains small. However, in a larger context, it attributed to 5% of global
deaths in 2015 according to the Global Burden of Disease Study(1).
can be histologically defined as the hyperinflation and loss of compliance of
air spaces distal to terminal bronchioles, in conjunction with the increased
rate of apoptosis of pneumocytes that line alveolar walls. Chronic bronchitis
effects the bronchi of the lungs and can be described as a continuous
productive cough with sputum production for a period of at least three months,
occurring over two consecutive years.
smoking exposes lung tissues to large quantities noxious chemicals (2), and in the instance of COPD, warrants an atypical
inflammatory response. Neutrophilic inflammation
is a characteristic hallmark of COPD (3).
Exposure of lung
tissue to noxious chemicals, including reactive oxygen species, causes
epithelial cell activation due contact with inflammatory mediators, which
results in the secretion of chemotactic cytokines, including tumour necrosis factor
alpha, interleukin-1 and interleukine-8, (IL-8) (4). Simultaneously, alveolar
macrophage stimulation in response to cigarette smoke occurs with resulting
secretion of leukotriene B4, IL-8 and neutrophil chemotactic factors (5). These cytokines result in the increased
recruitment of a form of granulocyte called a neutrophil.
Macrophages and neutrophils secrete serine proteases