Effect of obstructive sleep apnea on immunity in cases of chronic rhinosinusitis with nasal polyp.

xlomafota13 shared this article with you from Inoreader Effect of obstructive sleep apnea on immunity in cases of chronic rhinosinusitis with nasal polyp. Via pubmed: "clin exp otorhinola... Related Articles Effect of obstructive sleep apnea on immunity in cases of chronic rhinosinusitis with nasal polyp. Clin Exp Otorhinolaryngol. 2021 Jan 19;: Authors: Kim DK, Lee BC, Park KJ, Son GM Abstract Objective: Chronic rhinosinusitis (CRS) with nasal polyp (wNP) is a more severe inflammatory form of CRS that often coexists with obstructive sleep apnea (OSA). However, little is known the relationship between OSA and immunologic profile on patients with CRSwNP. We aimed to investigate the immune profile of patients with CRSwNP according to OSA severity. Methods: This study included 63 patients with CRSwNP and nine control subjects. Protein levels of inflammatory mediators were determined using multiplex immunoassay. All patients underwent standard polysomnography. Results: We found that, in patients with eosinophilic CRSwNP (ECRSwNP), IL-6 and CXCL-1 (type 1 immune-related markers) were upregulated in cases of moderate-to-severe OSA. Additionally, IL-4, IL-13, CCL-11, CCL-24 (type 2 immune-related markers), and IL-17A (type 3 immune-related marker) were increased in patients with moderate-to-severe OSA. Though there were no significant differences in type 1, 2, or 3 immune-related markers among patients with non-eosinophilic CRSwNP (NECRSwNP) according to the severity of OSA, TGF--β expression was increased in those with moderate-to-severe OSA. Furthermore, in ECRSwNP with moderate-to-severe OSA, associations were detected between serum markers and some upregulated inflammatory markers. Conclusion: Our findings revealed that OSA may increase the heterogeneity of immune profiles (types 1, 2, and 3) in patients with ECRSwNP but not in those with NECRSwNP. PMID: 33541034 [PubMed - as supplied by publisher] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.