Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/145440
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dc.titleEFFECT AND UNDERLYING MECHANISMS OF INTERLEUKIN-13 (IL-13) ON THE BIOLOGICAL FUNCTIONS OF NASAL EPITHELIUM
dc.contributor.authorLIU JING
dc.date.accessioned2018-07-31T18:01:03Z
dc.date.available2018-07-31T18:01:03Z
dc.date.issued2017-08-08
dc.identifier.citationLIU JING (2017-08-08). EFFECT AND UNDERLYING MECHANISMS OF INTERLEUKIN-13 (IL-13) ON THE BIOLOGICAL FUNCTIONS OF NASAL EPITHELIUM. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/145440
dc.description.abstractIL-13 is a key Th2 cytokine that acts as an important mediator in airway inflammation and remodeling. However, previous studies do not fully address the question on IL-13 initiation of airway inflammation and remodeling in nasal mucosa. In order to explore the role of IL-13 in upper airway, we use primary hNECs derived from hNESPCs, forming pseudo stratified layers in ALI culture. The hNECs model largely mimics the nasal epithelium in vivo. Our data demonstrate that IL-13 affects ciliated cells via the inhibition of ciliogenesis associated maker FOXJ1’s expression and interference on CP110 translocation. IL-13Rα2 has an important role in IL-13 induced mucus overproduction by upregulating MUC5AC expression and mucociliary dysfunctions through the activation of ERK1/2. IL-13Rα2 may contribute to airway inflammation and aberrant remodeling which are the main pathological features of CRSwNP. More importantly, IL-13 receptors and ERK1/2 pathways are attractive targets for therapeutic intervention in airway inflammatory disease.
dc.language.isoen
dc.subjectIL-13, Cilia, MUC5AC,ERK1/2,nasal mucosal inflammation, remodeling
dc.typeThesis
dc.contributor.departmentOTOLARYNGOLOGY
dc.contributor.supervisorWANG DE YUN
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
dc.identifier.orcid0000-0002-7511-0680
Appears in Collections:Ph.D Theses (Open)

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