The Prevalence of Subtypes of Type 2 Inflammation in an Unselected Population of Patients with Severe Asthma

Abstract

With the introduction of different targeted therapies for type 2 (T2)-high asthma, there is an urgent need for markers to guide the choice of treatment. T2-high asthma includes different clinical phenotypes of asthma, but the prevalence and impact of activation of different T2 inflammatory pathways is unknown. To describe the level of coexpression of clinically available T2 inflammatory markers in patients with severe asthma, and the relationship with clinical characteristics and comorbidities. Patients with severe asthma according to European Respiratory Society/American Thoracic Society guidelines were examined prospectively including sputum induction and grouped according to T2 biomarkers: blood eosinophilia (≥0.3× 109/L), total IgE (≥150 U/mL), and fractional exhaled nitric oxide (≥25 parts per billion). We found 116 (70%) of the 166 patients to have at least 1 T2 biomarker elevated: 39% had 2 or more elevated biomarkers, whereas 31% had only 1 biomarker elevated. Concomitant airway and systemic eosinophilia was present in 28% of all patients, corresponding to half (53%) of the patients with either. Expression patterns of the T2 biomarkers were associated with differences in allergic sensitization and the coexistence of nasal polyposis. Most patients with severe asthma showed at least 1 T2 inflammatory trait. Coexpression of T2 biomarkers was highly heterogeneous, and different expression patterns were associated with distinct clinical characteristics.