論文

査読有り
2016年9月

High glucose-induced oxidative stress increases IL-8 production in human gingival epithelial cells

ORAL DISEASES
  • Y. Kashiwagi
  • ,
  • M. Takedachi
  • ,
  • K. Mori
  • ,
  • M. Kubota
  • ,
  • S. Yamada
  • ,
  • M. Kitamura
  • ,
  • S. Murakami

22
6
開始ページ
578
終了ページ
584
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/odi.12502
出版者・発行元
WILEY

ObjectiveDiabetes is often associated with increased prevalence and severity of periodontal disease. We hypothesized that gingival epithelial cells modify periodontal disease progression and predicted that hyperglycemia would activate an inflammatory response in human gingival epithelial cells (HGECs).
Materials and MethodsWe tested our hypothesis in immortalized HGECs (epi 4 cells) isolated from periodontal tissue and transfected with the simian virus 40 T antigen. The epi 4 cells were cultured in high (25mM, HG) and normal (6mM, NG) glucose conditions.
ResultsThe epi 4 cells showed increased interleukin-8 (IL-8) protein secretion and mRNA expression when cultured in HG, compared with in NG. These effects were not associated with increased cell proliferation and were not observed in a hyperosmolar control group (normal glucose with 19mM mannitol). Increased IL-8 secretion in HG was inhibited by pretreatment with an antioxidant, N-acetylcysteine, or a protein kinase C inhibitor, Ro31-8220. Hyperglycemia did not affect IL-8 secretion by gingival fibroblasts or periodontal ligament cells. In epi 4 cells, hyperglycemia also induced expression of toll-like receptor 2 (TLR2) but not TLR4.
ConclusionThese findings suggest a potential participation of epithelial cells in periodontal disease during diabetes by evoking an excessive host inflammatory response.

リンク情報
DOI
https://doi.org/10.1111/odi.12502
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000381044200017&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/odi.12502
  • ISSN : 1354-523X
  • eISSN : 1601-0825
  • Web of Science ID : WOS:000381044200017

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