| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| 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.
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