| Project/Area Number |
13672001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Conservative dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NAKANISHI Tadashi Tokushima Univ., School of Dentistry Assistant professor, 歯学部附属病院, 講師 (00217770)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Hirotoshi Okayama Univ., Operative Dent., Instructor, 大学院・医歯学総合研究科, 助手 (70294709)
SUGE Toshiyuki Tokushima Univ., School of Dentistry Instructor, 歯学部, 助手 (60243713)
NAKAE Hideaki Tokushima Univ., School of Dentistry Associate professor, 歯学部, 助教授 (30227730)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | pulpitis / MIP-3α / CCR6 / macrophage / endothelial cell / lymphocyte / chemokine / chemokine receptor / RT-PCR / ELISA / Streptococcus mutans / IL-1β / TNF-α / CD45RO / 免疫染色 |
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| Research Abstract |
Severe pulpitis resulted from dental caries is characterized by a marked inflammatory infiltrate such as lymphocytes. Little is known about the recruitment of these cells into the lesion of dental plup in carious teeth. Macrophage inflammatory protein-3α (MIP-3α), one of the CC chemokines, is known to attract CC chemokine receptor 6 (CCR6)-expressing T cells, and CCR6 is typically expressed on memory T cells.
Then, we ezamined the expression of MIP-3α Mrna by RT-PCR and the distribution of MIP-3α-positive and CCR6-positive cells by immunohistochemistry in human dental pulp. MIP-3α expression was observed in all of the inflamed pulp samples, and microvascular endothelial cells. Moreover, CCR6 expression was also observed in the infiltrating lymphocytes, predominantly memory phenotype T cells. In contrast, MIP-3α and CCR6 was scarcely detected in normal pulps.
We also examined the pattern of MIP-3α expression in endothelial cells stimulated by Streptococcus mutans or cytokine (IL-1 β or TNF α) in vitro. The level of MIP-3α increased in time- and dose-dependent manner, and that both cytokines strongly induced MIP-3α secretion compared with S. mutans.
These findings suggest that MIP-3α plays an important role in the advancement of pulpal inflammation via the recruitment of CCR6-expressing lymphocytes. Furthermore, this study indicate that endothelial cells may modulate the accumulation of lymphocytes through the MIP-3α production.
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