MISC

2013年

Characterization of IL-18 Expression and Release in the Pathogenesis of Chronic Rhinosinusitis

INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
  • Mitsuhiro Okano
  • ,
  • Tazuko Fujiwara
  • ,
  • Seiichiro Makihara
  • ,
  • Rumi Fujiwara
  • ,
  • Takaya Higaki
  • ,
  • Shin Kariya
  • ,
  • Yohei Noda
  • ,
  • Takenori Haruna
  • ,
  • Kazunori Nishizaki

160
3
開始ページ
275
終了ページ
286
記述言語
英語
掲載種別
DOI
10.1159/000341668
出版者・発行元
KARGER

Background: Interleukin-18 (IL-18) is a member of the IL-1 cytokine family that affects chronic inflammation. We sought to characterize IL-18 expression and investigate its release during chronic rhinosinusitis (CRS). Methods: The expression of IL-18 in nasal polyps (NPs) and uncinate tissues (UTs) from both CRS and non-CRS patients was examined via immunohistochemistry. After culturing dispersed NP cells (DNPCs) with or without various stimulations, IL-18 levels were measured in the culture supernatants. Furthermore, the effect of IL-18 neutralization on staphylococcus enterotoxin B (SEB)-induced cytokine production was also examined. Results: Similar expression of IL-18 in the epithelial layers was observed between the NPs and UTs. However, there was a significantly higher number of IL-18(+) cells in the lamina propria from NPs compared to UTs without CRS. This increased number was significantly correlated with the radiological severity of sinusitis and local eosinophilia. After the dispersion, IL-18 was spontaneously released by NP cells in a phase-dependent manner. While SEB, fungal antigens, and TLR agonists did not enhance the release, exposure to protease or one cycle of a freeze-and-thaw treatment did induce release of IL-18 from rested DNPCs. In addition, neutralization of IL-18 significantly suppressed SEB-induced IL-5, IL-13, and IFN-gamma, but not IL-17A production. Conclusions: These results suggest that the pro-inflammatory effect of IL-18 released by danger signals may be involved in the pathogenesis of CRS, which includes eosinophilic inflammation and NP formation, via the augmentation of both Th2- and Th1-associated cytokine production. Copyright (C) 2012 S. Karger AG, Basel

Web of Science ® 被引用回数 : 5

リンク情報
DOI
https://doi.org/10.1159/000341668
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000311489200007&DestApp=WOS_CPL

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