The role of TLR2 in NASH progression caused by P.gingivalis odontogenic infection

2015 Fiscal Year Final Research Report

• Project/Area Number: 26861574
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pathobiological dentistry/Dental radiology
• Research Institution: Hiroshima University
• Principal Investigator: Hisako Furusho 広島大学, 医歯薬保健学研究院, 助教 (00634461)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: TLR2 / NASH / P.gingivalis

Outline of Final Research Achievements

I aimed to clarify roles of TLR2 (a Pg-LPS receptor) in activating hepatocytes and macrophages (MΦ) caused by Pg-odontogenic infection. In vivo experiment, WT and TLR2KO mice were 8-week-fed by Chow Diet (CD) and High Fat Diet (HFD), then the half of each mice were infected Pg from pulp, compared to non-infected groups. After 6-week-infection, immunoexpression of TLR2 and Mac2-positive MΦ infiltrating area in liver were analyzed. In WT-HFD groups, TLR2-expression in liver and MΦ-infiltrating area was significantly increased, compared to WT-CD groups. However, in TLR2KO mice, MΦ-area was unchanged. In vitro experiment, I used human hepatocytes and MΦ cell lines. TLR2 inhibitor suppressed proinflammatory cytokine expression caused by Pg-LPS stimulation. In fatty liver, TLR2 is related to steatosis and recruitment of MΦ, and to increasing Pg-reactivity, cause of marked inflammation. It was shown the association between TLR2 and NASH progression.

Free Research Field

口腔病理学