Roles of allergic cytokine IL-33 in the exacerbation of chronic periodontitis

2016 Fiscal Year Final Research Report

• Project/Area Number: 25463225
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Tohoku University
• Principal Investigator: Tada Hiroyuki 東北大学, 歯学研究科, 講師 (70431632)
• Co-Investigator(Renkei-kenkyūsha): MATSUSHITA KENJI 国立研究開発法人国立長寿医療研究センター, 部長 (90253898)
• Research Collaborator: MATSUYAMA TAKASHI 鹿児島大学, 大学院医歯学総合研究科, 准教授 (40253900) ; SHIMAUCHI HIDETOSHI 東北大学, 大学院歯学研究科, 名誉教授 (70187425)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 慢性歯周炎 / Porphyromonas gingivalis / Interleukin-33 / 歯肉上皮細胞 / 歯肉上皮バリア破綻

Outline of Final Research Achievements

The cytokine IL-33 is constitutively expressed in epithelial cells and it augments Th2 cytokine-mediated inflammatory responses. We aimed to determine the role of the periodontal pathogen, Porphyromonas gingivalis, in the enhanced expression of IL-33 in human gingival epithelial cells. We detected IL-33 in inflamed gingival epithelium from patients with chronic periodontitis, and found that P. gingivalis increased IL- 33 expression in the cytoplasm of human gingival epithelial cells in vitro. P. gingivalis gingipain-null mutant KDP136 did not induce IL-33 expression. A small interfering RNA for protease-activated receptor-2 (PAR-2) as well as inhibitors of phospholipase C, p38 and NF-κB inhibited the expression of IL-33 induced by P. gingivalis. These results indicate that the PAR-2/IL-33 axis is promoted by P. gingivalis infection in human gingival epithelial cells through a gingipain-dependent mechanism.

Free Research Field

口腔微生物学・免疫学