Bronchiectasis in severe asthma is associated with eosinophilic airway inflammation and activation
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Bronchiectasis in severe asthma is associated with eosinophilic airway inflammation and activation. / Frøssing, Laurits; Von Bülow, Anna; Porsbjerg, Celeste.
In: ERJ Open Research, Vol. 8, 2022, p. 252.Research output: Contribution to journal › Conference abstract in journal › Research › peer-review
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T1 - Bronchiectasis in severe asthma is associated with eosinophilic airway inflammation and activation
AU - Frøssing, Laurits
AU - Von Bülow, Anna
AU - Porsbjerg, Celeste
PY - 2022
Y1 - 2022
N2 - 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.
AB - 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.
U2 - 10.1183/23120541.LSC-2022.252
DO - 10.1183/23120541.LSC-2022.252
M3 - Conference abstract in journal
VL - 8
SP - 252
JO - ERJ Open Research
JF - ERJ Open Research
SN - 2312-0541
ER -
ID: 344850271