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Dual oxidase 2 is essential for the toll-like receptor 5-mediated inflammatory response in airway mucosa

Title
Dual oxidase 2 is essential for the toll-like receptor 5-mediated inflammatory response in airway mucosa
Authors
Joo J.-H.Ryu J.-H.Kim C.-H.Kim H.J.Suh M.-S.Kim J.-O.Chung S.Y.Lee S.N.Kim H.M.Bae Y.S.Yoon J.-H.
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2012
Journal Title
Antioxidants and Redox Signaling
ISSN
1523-0864JCR Link
Citation
vol. 16, no. 1, pp. 57 - 70
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Aims: Airway mucosa is constantly exposed to various airborne microbes, and epithelial host defense requires a robust innate immunity. Recently, it has been suggested that NADPH oxidase (NOX) isozymes serve functional roles in toll-like receptor (TLR)-mediated innate immune responses. However, the molecular mechanism between TLR and NOX-mediated reactive oxygen species (ROS) production in human airway mucosa has been poorly understood. Results: Here, we show that flagellin-induced ROS generation is dependent on dual oxidase 2 (DUOX2) activation, which is regulated by [Ca 2+] i mobilization in primary normal human nasal epithelial (NHNE) cells. Interestingly, we observed that silencing of DUOX2 expression in NHNE cells and nasal epithelium of Duox2 knockout mice failed to trigger mucin and MIP-2α production upon challenging flagellin. Innovation: Our observation in this study reveals that flagellin-induced hydrogen peroxide (H 2O 2) generation is critical for TLR5-dependent innate immune responses, including IL-8 production and MUC5AC expression in the nasal epithelium. Furthermore, DUOX2-mediated H 2O 2 generation activated by the flagellin-TLR5 axis might serve as a novel therapeutic target for infectious inflammation diseases in the airway tract. Conclusion: Taken together, we propose that DUOX2 plays pivotal roles in TLR5-dependent inflammatory response of nasal airway epithelium. © 2012 Mary Ann Liebert, Inc.
DOI
10.1089/ars.2011.3898
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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