Background: Bronchiectasis is a common co-morbidity in severe asthma; causative pathogenic mechanisms are not fully understood but may differ from other causes of bronchiectasis. The role of eosinophilic airway inflammation; a classic feature of asthma predominantly driven by IL-5 and IL-13; in bronchiectasis is unclear but association to disruption of the airway epithelium through eosinophil degranulation and increased mucus production is plausible.

Objective: To describe the prevalence of bronchiectasis in an unselected population of patients with severe asthma, and the association with the airway eosinophilic inflammation and activation.

Methods: All patients with severe asthma according to ERS/ATS criteria attending four respiratory clinics over a one-year period were included. All patients underwent HRCT and induced sputum was collected and analyzed for a cell-differential count and free eosinophilic granules (FEGs). Airway mRNA expression of T2 inflammatory pathways was assessed in sputum.

Results: A total of 108 patients were included. Bronchiectasis was present in 31% of patients with severe asthma and half (52%) of these patients had airway eosinophilia whereas only 16% of patients without bronchiectasis had airway eosinophilia. Patients with bronchiectasis had a significantly higher sputum eosinophil count (5.3 vs. 0.8, p=0.001) as well as more extensive eosinophil degranulation, compared to those without bronchiectasis , suggesting a higher degree of eosinophil activation.

Conclusion: Bronchiectasis in severe asthma was associated with eosinophilic airway inflammation and eosinophilic degranulation while we found no relation to IL-13 associated clinical or molecular markers.