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Immune Netw. 2019 Feb 4;19(1):e5. doi: 10.4110/in.2019.19.e5. eCollection 2019 Feb.

The Role of Autophagy in Eosinophilic Airway Inflammation.

Lee J1, Kim HS1,2,3.

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1
Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
2
Department of Microbiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
3
Stem Cell Immunomodulation Research Center (SCIRC), Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

Abstract

Autophagy is a homeostatic mechanism that discards not only invading pathogens but also damaged organelles and denatured proteins via lysosomal degradation. Increasing evidence suggests a role for autophagy in inflammatory diseases, including infectious diseases, Crohn's disease, cystic fibrosis, and pulmonary hypertension. These studies suggest that modulating autophagy could be a novel therapeutic option for inflammatory diseases. Eosinophils are a major type of inflammatory cell that aggravates airway inflammatory diseases, particularly corticosteroid-resistant inflammation. The eosinophil count is a useful tool for assessing which patients may benefit from inhaled corticosteroid therapy. Recent studies demonstrate that autophagy plays a role in eosinophilic airway inflammatory diseases by promoting airway remodeling and loss of function. Genetic variant in the autophagy gene ATG5 is associated with asthma pathogenesis, and autophagy regulates apoptotic pathways in epithelial cells in individuals with chronic obstructive pulmonary disease. Moreover, autophagy dysfunction leads to severe inflammation, especially eosinophilic inflammation, in chronic rhinosinusitis. However, the mechanism underlying autophagy-mediated regulation of eosinophilic airway inflammation remains unclear. The aim of this review is to provide a general overview of the role of autophagy in eosinophilic airway inflammation. We also suggest that autophagy may be a new therapeutic target for airway inflammation, including that mediated by eosinophils.

KEYWORDS:

Airway inflammation; Autophagy; Eosinophil

Conflict of interest statement

Conflict of Interest: The authors declare no potential conflicts of interest.

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