Project/Area Number |
14571746
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Morphological basic dentistry
|
Research Institution | Meikai University |
Principal Investigator |
OCHIAI Kuniyasu Meikai Univ., Sch. Of Dent., Professor, 歯学部, 教授 (50095444)
|
Co-Investigator(Kenkyū-buntansha) |
TAGAWA Yumi Meikai Univ., Sch. Of Dent., Research assist., 歯学部, 助手 (20348189)
TAKESHITA Akira Meikai Univ., Sch. Of Dent., Assist. Professor, 歯学部, 講師 (70236454)
AMANO Shigeru Meikai Univ., Sch. Of Dent., Asso. Professor, 歯学部, 助教授 (90167958)
OCHIAI Kurita tomoko Nihon Univ., Sch. of Dent. at Matsudo, Assist. Professor, 松戸歯学部, 講師 (20130594)
|
Project Period (FY) |
2002 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
Keywords | Periodontitis / Anaerobic bacteria. / Apoptosis / Fatty acids / Butyric acid / T-cell Fibroblast / Adhesion molecules / 嫌気性菌 / 歯周病 |
Research Abstract |
We have previously demonstrated that human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via proinflammatory cytokines such as IL-6 and IL-11, which are produced by fibroblasts stimulated with butyric acid. In this study, we determined if T cell adhesion to human gingival fibroblasts influenced the susceptibility of T cells to butyric acid-induced apoptosis. We have shown that the number of Jurkat T cells adherent to gingival fibroblasts (Gin 1 cells) was significantly increased by the addition of butyric acid. All Jurkat cells that adhered to Gin-1 cells remained viable, while the non-adherent Jurkat cells dropped into apoptosis. The increase in T cell adhesion to fibroblasts was also observed when Jurkat cells, but not Gin 1 cells, were pretreated with butyric acid. CD44, very late antigen (VLA)-2 and VLA-5 but not leukocyte function-associated antigen 1 (LFA-1) and VLA-4 expressions on Jurkat cells were increased following treatment with butyric acid. Furthermore, pretreatment of butyric acid-sensitized Jurkat cells with monoclonal antibodies against CD44, VLA-2 and VLA-5, but not LFA-1 and VLA-4, followed by co-culture with Gin-1 cells abrogated T-cell adhesion to fibroblasts. These results indicate that the T-cell adherence to fibroblasts is enhanced by butyric acid, and that butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts through an interaction with the adhesion molecules CD44, VLA-2 and VLA-5 expressed on T cells stimulated with butyric acid.
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