title: Eosinophil apoptosis and the resolution of airway inflammation in asthma.
abstract: Asthma is accompanied by the accumulation of potentially damaging eosinophils within inflamed airways. How eosinophils may be removed from the airways is not clear. The phagocytic removal of eosinophils in vitro requires that they undergo apoptosis, a form of cell death. We postulated that eosinophil apoptosis may occur in vivo, promoting the removal of airway eosinophils and the resolution of inflammation in asthma. We examined eosinophil apoptosis in sputum samples obtained from 11 subjects during an asthma exacerbation and 2 wk after corticosteroid treatment of the exacerbation. Airway function improved following corticosteroid treatment, and eosinophilic inflammation subsided, with significant decreases occurring in the number of airway eosinophils and the percentage of activated eosinophils. The proportion of apoptotic airway eosinophils increased significantly following corticosteroid treatment, and eosinophil products were apparent within macrophages. Our findings indicate that eosinophil apoptosis is clinically relevant in asthma. Apoptosis may represent a mechanism that promotes the resolution of eosinophilic inflammation in asthma.
authors.affiliation: Airway Research Centre, John Hunter Hospital, Newcastle, New South Wales, Australia.
authors.forename: K L
authors.initials: KL
authors.lastname: Woolley
authors.forename: P G
authors.initials: PG
authors.lastname: Gibson
authors.forename: K
authors.initials: K
authors.lastname: Carty
authors.forename: A J
authors.initials: AJ
authors.lastname: Wilson
authors.forename: S H
authors.initials: SH
authors.lastname: Twaddell
authors.forename: M J
authors.initials: MJ
authors.lastname: Woolley
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D017209:Apoptosis; D001249:Asthma / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D001980:Bronchi / Q000473:pathology*; D004804:Eosinophils / Q000473:pathology / Q000502:physiology* / Q000648:ultrastructure; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010366:Peak Expiratory Flow Rate
chemical_list: D000305:Adrenal Cortex Hormones