Allergy Asthma Immunol Res.  2019 May;11(3):320-329. 10.4168/aair.2019.11.3.320.

Which Factors Associated With Activated Eosinophils Contribute to the Pathogenesis of Aspirin-Exacerbated Respiratory Disease?

Affiliations
  • 1Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea. hspark@ajou.ac.kr

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.

Keyword

Eosinophils; epithelium; therapy

MeSH Terms

Biological Products
Cytokines
Eosinophilia
Eosinophils*
Epithelium
Humans
Inflammation
Lung
Mucous Membrane
Biological Products
Cytokines

Figure

  • Figure Therapeutic approach to the management of AERD patients. A leukotriene receptor antagonist attenuates asthma exacerbation caused by cysteinyl leukotriene production. An anti-IL-5/IL-5 receptor antibody inhibits eosinophil activation to release several mediators. An anti-TSLP or IL-33 antibody may potentially reduce type 2 immune responses associated with eosinophilic inflammation. AERD, aspirin-exacerbated respiratory disease; IL, interleukin; NSAID, nonsteroidal anti-inflammatory drug; TSLP, thymic stromal lymphopoietin; SPD, surfactant protein D; CysLT, cysteinyl leukotriene.


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