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COPD is a chronic respiratory disease characterised by progressive airway inflammation, yet traditional therapies, such as bronchodilators and corticosteroids, do little to target the underlying biology.3-5
Every exacerbation causes lasting lung damage, contributing to disease progression and increasing a patient’s risk of hospitalisation or death, as well as significantly impacting their ability to live their life.6-9
In addition, every exacerbation increases the risk of the next exacerbation.6
Up to 51% of patients with a history of exacerbations continue to suffer from exacerbations, even with current therapies.*10
*moderate or severe.
Following exposure to tobacco smoke, bacteria and viruses, damaged lung epithelial cells release a number of different alarmins, one of which is IL-33 - an ST2 receptor-mediated cytokine.13,17
Binding of IL-33 to the ST2 receptor, expressed across a broad range of immune cells, initiates and amplifies multiple downstream inflammatory pathways that contribute to both neutrophilic (Type 1 and 3) and eosinophilic (Type 2) inflammation.13,17
Studies to explore the impact of targeting the ST2/IL-33 pathway in a broad population of COPD patients are ongoing.18–24
References