RT Journal Article
SR Electronic
T1 Do eosinophils contribute to oxidative stress in mild asthma?
JF ERJ Open Research
JO erjor
FD European Respiratory Society
SP PP232
DO 10.1183/23120541.lungscienceconference-2019.PP232
VO 5
IS suppl 2
A1 Linsey E. S. de Groot
A1 Yanaika S. Sabogal Piñeros
A1 Suzanne M. Bal
A1 Marianne A. Van De Pol
A1 Jörg Hamann
A1 Peter J. Sterk
A1 Wim Kulik
A1 René Lutter
YR 2019
UL http://openres.ersjournals.com/content/5/suppl_2/PP232.abstract
AB Loss of asthma control and asthma exacerbations are predominantly triggered by respiratory viral infections and characterized by eosinophilic airway inflammation and increased oxidative stress. Production of reactive oxygen species is a key feature of activated eosinophils and a link between eosinophils and oxidative stress during exacerbations is thus likely. We investigated whether attenuation of eosinophil numbers and activation using mepolizumab (anti-IL-5) impacts oxidative stress in stable and virus-induced worsening of asthma.Patients with mild asthma received one high dose of mepolizumab or placebo and after two weeks were subjected to rhinovirus 16 (RV16) infection. Exhaled breath condensate (EBC) and plasma was collected at baseline, after treatment and after RV16 challenge and levels of malondialdehyde (MDA), nitrotyrosine, bromotyrosine, chlorotyrosine, dityrosine and asymmetric dimethylarginine (ADMA) were measured using mass spectrometry.Baseline oxidative stress was not significantly different between the mepolizumab and placebo group and did not change upon treatment. EBC MDA near-significantly and nitrotyrosine significantly increased after virus exposure in the placebo group, but not in the mepolizumab group. When stratified for patients with high and low eosinophil counts, MDA levels significantly increased in the high eosinophilic placebo group only. No significant differences were observed after RV16 for any of the biomarkers in plasma.We have demonstrated that in mild asthma eosinophils may contribute to local oxidative stress, but only after RV16-induced loss of asthma control and not in stable disease.FootnotesCite this article as: ERJ Open Research 2019; 5 : Suppl. 2, PP232.This is an ERS Lung Science Conference abstract. No full-text version is available. Further material to accompany this conference is available at www.ers-education.org (ERS member access only).