PMID- 23075512
OWN - NLM
STAT- MEDLINE
DCOM- 20130419
LR  - 20181202
IS  - 1423-0097 (Electronic)
IS  - 1018-2438 (Linking)
VI  - 160
IP  - 3
DP  - 2013
TI  - Characterization of IL-18 expression and release in the pathogenesis of chronic 
      rhinosinusitis.
PG  - 275-86
LID - 10.1159/000341668 [doi]
AB  - 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.
CI  - Copyright (c) 2012 S. Karger AG, Basel.
FAU - Okano, Mitsuhiro
AU  - Okano M
AD  - Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate 
      School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. 
      mokano@cc.okayama-u.ac.jp
FAU - Fujiwara, Tazuko
AU  - Fujiwara T
FAU - Makihara, Seiichiro
AU  - Makihara S
FAU - Fujiwara, Rumi
AU  - Fujiwara R
FAU - Higaki, Takaya
AU  - Higaki T
FAU - Kariya, Shin
AU  - Kariya S
FAU - Noda, Yohei
AU  - Noda Y
FAU - Haruna, Takenori
AU  - Haruna T
FAU - Nishizaki, Kazunori
AU  - Nishizaki K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121017
PL  - Switzerland
TA  - Int Arch Allergy Immunol
JT  - International archives of allergy and immunology
JID - 9211652
RN  - 0 (Antibodies, Blocking)
RN  - 0 (Cytokines)
RN  - 0 (Enterotoxins)
RN  - 0 (Interleukin-18)
RN  - 39424-53-8 (enterotoxin B, staphylococcal)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Blocking/pharmacology
MH  - Cells, Cultured
MH  - Chronic Disease
MH  - Cytokines/metabolism
MH  - Enterotoxins/immunology
MH  - Female
MH  - Gene Expression/immunology
MH  - Humans
MH  - Interleukin-18/*immunology
MH  - Lymphocyte Activation/drug effects
MH  - Male
MH  - Middle Aged
MH  - Nasal Mucosa/*immunology
MH  - Nasal Polyps/complications/*immunology
MH  - Rhinitis/complications/*immunology
MH  - Sinusitis/complications/*immunology
EDAT- 2012/10/19 06:00
MHDA- 2013/04/23 06:00
CRDT- 2012/10/19 06:00
PHST- 2012/01/04 00:00 [received]
PHST- 2012/07/06 00:00 [accepted]
PHST- 2012/10/19 06:00 [entrez]
PHST- 2012/10/19 06:00 [pubmed]
PHST- 2013/04/23 06:00 [medline]
AID - 000341668 [pii]
AID - 10.1159/000341668 [doi]
PST - ppublish
SO  - Int Arch Allergy Immunol. 2013;160(3):275-86. doi: 10.1159/000341668. Epub 2012 
      Oct 17.