The role of TLR2 in NASH progression caused by P.gingivalis odontogenic infection
Project/Area Number |
26861574
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | Hiroshima University |
Principal Investigator |
Hisako Furusho 広島大学, 医歯薬保健学研究院, 助教 (00634461)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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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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Keywords | TLR2 / NASH / P.gingivalis / 歯性感染 |
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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Report
(3 results)
Research Products
(8 results)
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[Journal Article] Osteodystrophy in Cholestatic Liver Diseases Is Attenuated by Anti-γ-Glutamyl Transpeptidase Antibody.2015
Author(s)
Kawazoe Y, Miyauchi M, Nagasaki A, Furusho H, Yanagisawa S, Chanbora C, Inubushi T, Hyogo H, Nakamoto T, Suzuki K, Moriwaki S, Tazuma S, Niida S, Takata T.
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Journal Title
Related Report
Peer Reviewed / Open Access
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