The chronic airways diseases, asthma and Chronic Obstructive Pulmonary Disease (COPD), are highly prevalent conditions causing significant morbidity and mortality worldwide. Both are acknowledged to be heterogeneous with respect to clinical presentation, prognosis and driving mechanisms.1 Type-2 airway inflammation is arguably the most important and treatable underlying mechanism to identify,1 as it can be successfully targeted by inhaled and systemic corticosteroids,2 3 or by biological therapies (anti-IL5/IL5R, anti-IL4/IL4R/IL13 and anti-TSLP) in patients with refractory disease.4 Type-2 airway inflammation is not only a key driver of morbidity and mortality but can be identifiable with two easily accessible biomarkers: the peripheral blood eosinophil count (BEC) and fractional exhaled nitric oxide (FeNO).5

There is consistent and compelling evidence linking raised type-2 biomarkers to exacerbation frequency6 7 and increased risk of exposure to oral corticosteroids with their associated toxicity leading to ‘people remodelling’8 ; and that treatments which reduce type-2 inflammation have a significant positive impact on exacerbation risk1 4 9 and mortality.10 However, there has been less focus on the role of type-2 inflammation in the airway remodelling associated with lung function decline and progressive airflow limitation.

In this issue of Thorax, Çolak et al 11 have used a large and well-characterised Danish population-based cohort followed for 10 years, to investigate the relationship between BEC (measured before and after the observation period in 15 605 individuals), FeNO (measured in a subset of 2853 patients after the observation period) and …