A peptide derived from rice inhibits alveolar bone resorption via suppression of inflammatory cytokine production

Yukari Aoki-Nonaka, Koichi Tabeta, Mai Yokoji, Aoi Matsugishi, Yumi Matsuda, Naoki Takahashi, Benso Sulijaya, Hisanori Domon, Yutaka Terao, Masayuki Taniguchi, Kazuhisa Yamazaki

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

Background: Periodontitis is an inflammatory disease that results in alveolar bone resorption due to inflammatory cytokine production induced by bacterial antigens such as lipopolysaccharides (LPS). Here, the preventive effect of the Amyl-1-18 peptide derived from rice in an experimental model of periodontitis and the effect on the anti-inflammatory response were assessed. Methods: Alveolar bone resorption, gene transcription of proinflammatory cytokines in the gingiva, and the endotoxin level in the oral cavity were evaluated after oral administration of the Amyl-1-18 peptide for 14 days using a ligature-induced periodontitis model in mice. Additionally, murine macrophages were incubated with LPS of Escherichia coli or Porphyromonas gingivalis in the presence of Amyl-1-18 to analyze the suppressive effects of Amyl-1-18 on the cell signaling pathways associated with proinflammatory cytokine production, including inflammasome activities. Results: Oral administration of Amyl-1-18 suppressed alveolar bone resorption and gene transcription of interleukin (il)6 in the gingiva of the periodontitis model, and decreased endotoxin levels in the oral cavity, suggesting modulation of periodontal inflammation by inhibition of endotoxin activities in vivo. Also, Amyl-1-18 suppressed IL-6 production induced by LPS and recombinant IL-1β in macrophages in vitro but had no effect on inflammasome activity. Conclusions: The Amyl-1-18 peptide from rice inhibited alveolar bone destruction in mouse periodontitis model via suppressing inflammatory cytokine production induced by LPS. It was suggested that Amyl-1-18 peptide has anti-inflammatory property against LPS, not only by neutralization of LPS and subsequent inhibition of nuclear factor-κB signaling but also by inhibition of the IL-1R-related signaling cascade.

Original languageEnglish
Pages (from-to)1160-1169
Number of pages10
JournalJournal of Periodontology
Volume90
Issue number10
DOIs
Publication statusPublished - 1 Oct 2019

Keywords

  • anti-inflammatory agents
  • interleukin-1beta
  • lipopolysaccharides
  • macrophages
  • periodontitis

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