Autophagy regulates DUOX1 localization and superoxide production in airway epithelial cells during chronic IL-13 stimulation.

ABSTRACT: The airway epithelium is a broad interface with the environment, mandating well-orchestrated responses to properly modulate inflammation. Classically, autophagy is a homeostatic pathway triggered in response to external cellular stresses, and is elevated in chronic airway diseases. Recent findings highlight the additional role of autophagy in vesicle trafficking and protein secretion, implicating autophagy pathways in complex cellular responses in disease. Th2 cytokines, IL-13 and IL-4, are increased in asthma and other airway diseases contributing to chronic inflammation. Previously, we observed that IL-13 increases reactive oxygen species (ROS) in airway epithelial cells in an autophagy-dependent fashion. Here, we tested our hypothesis that autophagy is required for IL-13-mediated supero

SUBMITTER: Dickinson JD 

PROVIDER: S-EPMC5635347 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature