Which Factors Associated With Activated Eosinophils Contribute to the Pathogenesis of Aspirin-Exacerbated Respiratory Disease?
Allergy, Asthma & Immunology Research
; : 320-329, 2019.
Article
in En
| WPRIM
| ID: wpr-830105
Responsible library:
WPRO
ABSTRACT
Eosinophils have long been recognized as a central effector cell in the lungs of asthmatic patients. They contribute to airway inflammation and remodeling through releasing several molecules such as cytokines, granule proteins, lipid mediators and extracellular traps/vesicles. Repeated evidence reveals that intense eosinophil infiltration in upper and lower airway mucosae contributes to the pathogenesis of aspirin-exacerbated respiratory disease (AERD). Persistent eosinophilia is found to be associated with type 2 immune responses, cysteinyl leukotriene overproduction and eosinophil-epithelium interactions. This review highlights recent findings about key mechanisms of eosinophil activation in the airway inflammation of AERD. In addition, current biologics (targeting type 2 immune responses) were suggested to control eosinophilic inflammation for AERD patients.
Full text:
1
Database:
WPRIM
Type of study:
Etiology_studies
Language:
En
Journal:
Allergy, Asthma & Immunology Research
Year:
2019
Document type:
Article