Nucleotide-Binding Oligomerization Domain-Like Receptor 3 Inflammasome Inhibition by MCC950 Reduces the Lipopolysaccharide-Induced Interleukin-1β in Cultured Dispersed Nasal Polyp Cells

서지정보

· 발행기관 : 대한이비인후과학회
· 수록지 정보 : 대한이비인후-두경부외과학회지 / 63권 / 5호 / 206 ~ 215페이지
· 저자명 : 박수경, 한예녕, 허준, 연선희, 이성복, 송근호, 변진희, 나기상, 김용민

초록

Background and Objectives The nucleotide-binding oligomerization domain-like receptor(NLRP) 3 is known as a member of the NLR family, and it has been confirmed that the NLRP3inflammasome is associated with various diseases such as asthma, inflammatory bowel disease,metabolic disorders and multiple sclerosis, as well as other auto-immune and auto-inflammatorydiseases. However, the role of NLRP3 in chronic rhinosinusitis with nasal polyps (CRSwNP)has not yet been explored.
Subjects and Method Forty-four specimens of nasal polyps and 25 specimens of uncinateprocesses were collected from patients with chronic rhinosinusitis with nasal polyps, and 25specimens of uncinate tissues were collected from patients who underwent other rhino-surgeries.
The western blot assay was employed to analyze the expression of NLRP3; interleukin (IL)-1βand IL-17A were detected using immunohistochemistry and real-time polymerase chain reaction.
The production of lipopolysaccharide (LPS) induced IL-1β and IL-17A with or without theNLRP3 inflammasome inhibitor (MCC950) was measured using an enzyme linked immunosorbentassay in cultured dispersed nasal polyp cells.
Results NLRP3 showed a high level of expression in nasal polyps than in the control group(p<0.01). The expression of IL-1β and IL-17A was significantly higher in nasal polyps in theCRSwNP group than in the control group (p<0.05). LPS-induced production of IL-1β was significantlysuppressed by treatment with the NLRP3 inflammasome inhibitor (p<0.05).
Conclusion The NLRP3 inflammasome plays an essential role in the pathogenesis of CRSwNP,and thus MCC950 can be considered a prospective therapeutic for NLRP3 inflammasome-mediatedinflammation in nasal polyps. Our data provide new evidence that IL-17A is involved in inflammasome-associated inflammation in nasal polyps.

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