Abstract
Chronic obstructive pulmonary disease (COPD) encompasses a spectrum of lung disorders that cause lung function decline. The degree by which lung function has decreased is used to classify disease severity and as a guide for escalated long-acting bronchodilator use. This strategy aims to modify symptoms but does not target the inflammatory processes that drive disease progression. COPD has distinct, but non-mutually exclusive, endotypes such as chronic bronchitis and emphysema.1 These endotypes each have unique pathogeneses, and diagnosis of COPD is often not consistent between individuals in terms of immunopathology.
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