| Project/Area Number |
12470473
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Aichi-Gakuin University |
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Principal Investigator |
NOGUCHI Toshihide Dept.of Periodontology, Sch.of Dent, Aichi-Gakuin Univ., Professor, 歯学部, 教授 (50014262)
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| Co-Investigator(Kenkyū-buntansha) |
MITANI Akio Dept.of Periodontology, Sch.of Dent, Aichi-Gakuin Univ., Assistant Professor, 歯学部, 助手 (50329611)
ISHIHARA Yuichi Dept.of Periodontology, Sch.of Dent, Aichi-Gakuin Univ., Assistant Professor, 歯学部, 講師 (50261011)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2000: ¥7,600,000 (Direct Cost: ¥7,600,000)
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| Keywords | Mucosal infection / IL-15 / γδT cell / Th1 / 上皮系サイトカイン |
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| Research Abstract |
To know the role of intraepithelial lymphocyte as an etiology of periodontal disease, the mechanism responsible for C57BL/6 as resistance mice and BALB/c as susceptibility mice to oral infection with Listeria monocytogenes were studied by comparing early IL-15 production in intestinal epithelial cells (i-EC).
After mice were inoculated p.o. with viable L. monocytogenes, the bacteria in liver, spleen, mesenteric lymph nodes (MLN) and Peyer's patch (PP) were counted on day 1, 3 or 5. C57BL/6 mice were shown higher level of resistance than BALB/c in all organs. To know the difference of these resistance, we investigate kinetics of the intestinal intraepithelial lymphocytes (i-IEL) during oral infection with L.monocytogenes. There were no significant difference in the absolute : nmber and the ratio of i-IEL subpopulations bearing CD8αα and CDαβ or TCRαβ and γδ on day 1, 3 and 5 after oral infection. Thus, these results suggest that oral infection with L.monocytogenes may not affect the subp
… More
opulation of i-IEL in each mice. Next, we investigate the difference of cytokines production in i-EC and i-IEL after oral infection. High levels of IL-15 mRNA and IL-15 protein in i-EC from C57BL/6 mice were expressed on day 1 after L.monocytogenes infection, whereas in i-EC from BALB/c mice, those were expressed very low. Concurrently, a amount of IFN-γ which was produced by i-IEL from C57BL/6 mice in response to CD3 stimulation were higher than by that from BALB/c mice. While the i-IEL from BALB/c mice produced a higher level of IL-4 upon CD3 stimulation than that of C57BL/6 mice. The toll-like receptor (TLR) 2 has been suggested as a receptor for bacterial lipoproteins from Mycobacteria or Gram-positive bacteria. The mRNA expression level of TLR2, which is recognized to mediate a partly signaling for IL-15 gene transcription, was increased in i-EC from C57BL/6 mice on day 1 after L.monocytogenes infection.
These results suggest that TLR2 expression regards difference of IL-15 production, and that the difference in early production of IL-15 by i-EC may at least partly underlie the difference in susceptibility to L.monocytogenes between C57BL/6 and BALB/c mice. Less
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