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Although 12 weeks is enough for morphologic regeneration of the ciliated epithelium after experimental sinusitis in rabbit maxillary sinuses, it does not appear long enough for full functional recovery. Restoration of CBFs does not equate to concurrent CWD restoration.

Of 970 patients, 50.3% had NSD. According to the Guyuron and Mladina classifications, type 2 (41.4%) and type 1 (35.4%) were most common, respectively. Among 64 patients who underwent septoplasty, the concordance rates with CT findings were 71.9% for the Guyuron classification and 50% for the Mladina classification. This difference was statistically significant (chi-squared test, p = 0.026).

BackgroundThe proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). However, the mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown.ObjectivesIn this study, we assessed the contribution of IL-17A to eosinophil-related inflammation via the CCL7/CCR3 pathway in experimental allergic rhinitis.MethodsIL-17A knockout (KO) and wild-type (WT) BALB/c mice were injected intraperitoneally and challenged intranasally with OVA to induce allergic rhinitis. Various parameters of the allergic response were evaluated, and mRNA and protein levels of CCL7 and CCR3 in nasal tissue and serum were compared between the two groups. The chemotactic response to CCL7 with or without IL-17A in bone marrow-derived eosinophils (bmEos) from BALB/c mice was measured.ResultsIn the allergic rhinitis model, IL-17A deficiency significantly decreased nasal symptoms, serum IgE levels, and eosinophil recruitment to the nasal mucosa. CCL7 and CCR3 mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice. BmEos showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence.ConclusionThe suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway.