Journal
CURRENT ALLERGY AND ASTHMA REPORTS
Volume 13, Issue 2, Pages 209-217Publisher
CURRENT MEDICINE GROUP
DOI: 10.1007/s11882-012-0328-6
Keywords
Chronic rhinosinusitis (CRS); Pathophysiology; Inflammation; Remodeling; Environmental factors; Nasal epithelium; Host defense mechanisms; Gene expression signatures; Regulatory T cells (T-reg); Glucocorticosteroids; Nasal polyps
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Funding
- National Medical Research Council (NMRC) [IRG10may086]
- Singapore Immunology Network (SIgN) of Singapore [SIgN 10-028]
- National Nature Science Foundation of China [81170897]
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Chronic rhinosinusitis (CRS) is a complex inflammatory disease with variable disease manifestation. Though external risk factors are associated with development and/or persistence of CRS, the host mucosal response is also important, as nasal epithelium acts as a physical and immune barrier. Under inflammatory stress, the nasal epithelium can undergo injury, followed by a rapid remodeling response ranging from epithelial hyperplasia, to goblet-cell metaplasia, to denudation, loss of cilia, fibrosis, and basement membrane thickening. Identification of gene expression signatures and molecular pathways in CRS pathogenesis have now begun to contribute significantly to a better understanding of the genetic and molecular alterations underlying CRS development and progression. Genetic studies are especially illuminating when multiple gene variants synergize within a permissive environmental context, and are expected to guide development of more effective therapeutic targets for CRS treatment.
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