Chronic Obstructive Pulmonary Disease (COPD) is an obstructive airwaysdisease, characterised by apartially reversible, but progressive worsening obstruction of airflow. COPD isan umbrella term which encompasses pulmonary emphysema and chronic bronchitis1. It is well-known that cigarette smoking isthe key risk-factor for an individual developing COPD. Despite the fact thatall cigarette smokers evoke a degree of inflammation and subsequently damage tothe airway epithelium, the number of individuals who consequentially developCOPD remains small. However, in a larger context, it attributed to 5% of globaldeaths in 2015 according to the Global Burden of Disease Study(1). Pulmonary emphysemacan be histologically defined as the hyperinflation and loss of compliance ofair spaces distal to terminal bronchioles, in conjunction with the increasedrate of apoptosis of pneumocytes that line alveolar walls. Chronic bronchitiseffects the bronchi of the lungs and can be described as a continuousproductive cough with sputum production for a period of at least three months,occurring over two consecutive years.
Long-term cigarettesmoking exposes lung tissues to large quantities noxious chemicals (2), and in the instance of COPD, warrants an atypicalinflammatory response. Neutrophilic inflammationis a characteristic hallmark of COPD (3). Exposure of lungtissue to noxious chemicals causes epithelial cell activation due contact withinflammatory mediators, which results in the secretion of chemotacticcytokines, including tumour necrosis factor alpha, interleukin-1 andinterleukine-8, (IL-8) (4). Simultaneously, alveolarmacrophage stimulation in response to cigarette smoke occurs with resultingsecretion of leukotriene B4, IL-8 and neutrophil chemotactic factors (5).
These cytokines result in the increasedrecruitment of a form of granulocyte called a neutrophil.
