Calprotectin Induces IL-6 and MCP-1 Production via Toll-Like Receptor 4 Signaling in Human Gingival Fibroblasts

DOI 機関リポジトリ NDLデジタルコレクション

書誌事項

タイトル
Calprotectin Induces IL-6 and MCP-1 Production via Toll-Like Receptor 4 Signaling in Human Gingival Fibroblasts
タイトル別名
  • カルプロテクチンは、ヒト歯肉線維芽細胞のTLR4を介してIL-6, MCP-1の産生を誘導する
  • Calprotectin/TLR4 induced induced-Cytokine Production
著者
西川, 泰史
著者別名
  • ニシカワ, ヤスフミ
  • Nishikawa, Yasufumi
著者
梶浦, 由加里
著者別名
  • カジウラ, ユカリ
  • Kajiura, Yukari
著者
Lew, Jung Hwan
著者
木戸, 淳一
著者別名
  • キド, ジュンイチ
  • Kido, Jun-ichi
著者
永田, 俊彦
著者別名
  • ナガタ, トシヒコ
  • Nagata, Toshihiko
著者
成石, 浩司
著者別名
  • ナルイシ, コウジ
  • Naruishi, Koji
学位授与大学
徳島大学
取得学位
博士（歯学）
学位授与番号
甲口第433号
学位授与年月日
2018-03-23

説明

Calprotectin, a heterodimer of S100A8 and S100A9 molecules, is associated with inflammatory diseases such as inflammatory bowel disease. We have reported that calprotectin levels in gingival crevicular fluids of periodontitis patients are significantly higher than in healthy subjects. However, the functions of calprotectin in pathophysiology of periodontitis are still unknown. The aim of this study is to investigate the effects of calprotectin on the productivity of inflammatory cytokines in human gingival fibroblasts(HGFs). The HGFs cell line CRL-2014®(ATCC) were cultured, and total RNAs were collected to examine the expression of TLR2/4 and RAGE mRNA using RT-PCR. After the cells were treated with S100A8, S100A9 and calprotectin, supernatants were collected and the levels of IL-6 and MCP-1 were measured using ELISA methods. To examine the intracellular signals involved in calprotectin-induced cytokine production, several chemical inhibitors were used. Furthermore, after the siRNA-mediated TLR4 down-regulated cells were treated with S100A8, S100A9 and calprotectin, the levels of IL-6 and MCP-1 were also measured. HGFs showed greater expression of TLR4 mRNA, but notTLR2 and RAGE mRNA compared with human oral epithelial cells. Calprotectin increased significantly the production of MCP-1 and IL-6 in HGFs, and the cytokine productions were significantly suppressed in the cells treated with MAPKs, NF-kBand TLR4inhibitors. Furthermore, calprotectin-mediated MCP-1 and IL-6 production were significantly suppressed in TLR4down-regulated cells. Taken together, calprotectin inducesIL-6 and MCP-1 production in HGFs via TLR4 signaling that involves MAPK and NF-kB, resulting in the progression of periodontitis.

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ