| Project/Area Number |
14571752
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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 |
Morphological basic dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
KOMIYAMA Kazuo Nihon University, School of Dentistry, Associate professor, 歯学部, 助教授 (00120452)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Oeal lichen planus / cytokine / mucosa / Dendritic cell / T-cell / NK cell / PLA2 / COX2 / Lichen planus / dendritic cell / Th1 cell / IL-2 / INFg / chemokine / RT-PCR / flowcytometor |
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| Research Abstract |
Oral lichen planus is difficult to cure with unknown etiology. The lesion is characterized histological by band-like T cells infiltration just under the basal cell layer of mucosal epithelium and Killer T cell infiltration into the basal cell layer, while certain mechanism of 'these cells infiltration were not clarified. We have developed a mouse experimental model of oral mucosal delayed type hyperplasia as a mimic of oral lichen planus. In this study, we evaluated the cells and cytokine involve OLP development the lesion for the development of useful treatment system. Our result clearly indicted that NK cell play key role for the early development of the lesion. NK cells deletion following asialo GM1 antibody treatment mouse that was clearly showed decrease the severity of DTH reaction due to the less number of lymphocytes recruitment. IL-2 and INF-γ are major cytokines involved in cell infiltration of the lesion. IL-2 revealed by standard expression at course of early lesion. These cell and cytokines regulate disease development. Another characteristic feature of the lesion is numerous dendritic cells (DC) infiltrate in to the epithelial layer. DC may also important cell elements for the controlling the OLP. We further examined cyclooxigenase 2 (COX2) and Phospholipase A2 expression of the OLP lesion, which relate to characteristic white color appearance on oral mucosa. COX2 over expression was paralleled to thickness of epithelium and amounts of prickle cells in the epithelium. Clear finding obtained that subgroup specific PLA2, PLA2-V and PLA2-X but not for PLA2-IIa, were identified in the basal cells of epithelium and macrophages. The results indicted prostanoid like prostaglandin E2 play a role for the epithelial cell repair following epithelial cells received damage by CD8 positive cell and NK cells. More over the COX2 over expression in the lesions may be related to malignant transformation of OLP.
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