Cell Adhesion Molecule Expression in Human Periodatitis
Project/Area Number |
05671591
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Conservative dentistry
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Research Institution | Tokyo Medical and Dental University (TMDU) |
Principal Investigator |
WATANABE Hisashi TMDU Periodontics Associate Professor, 歯学部, 助教授 (40143606)
|
Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Eiichi TMDU Periodontics Research Associate, 歯学部, 助手 (20242208)
|
Project Period (FY) |
1993 – 1994
|
Project Status |
Completed (Fiscal Year 1994)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | Cesll Adhesion Molecule / ICAM-1 / VCAM-1 / LFA-1 / Periodontal Disease / Serum Antibody Titer / サイトカイン / 歯周病原性細菌 / 成人性歯周炎 / 歯周炎 / 接着分子 / ELAM-1 / RT-PCR法 / IL-1β / mRNA |
Research Abstract |
Chronic inflammatory diseases caused by bacterial infection, including adult periodontitis (AP), are characterized by a local accumulation of activated inflammatory cells. We examined whether intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin (endothelial leukocyte adhesion molecule-1 ; ELAM-1) are involved in AP lesions. Gingival tissues from AP patients showed increased levels of these molecules mRNA,compared with those form normal healthy donors. Immunohistological analysis revealed that ICAM-1 was also expressed by gingival fibroblasts. Therefore, we investigated the expression and regulation of ICAM-1 on cultured human gingival fibroblasts (HGF). Cell surface ICAM-1 was upregulated on HGF under transcriptional control by exposure not only to IL-1b, TNF-a, or IFN-g but also to sonic extracts (SE) from periodontopathic bacteria (Porphromonas gingivalis and Prevotella intermedia) and LPS from Escherichia coli. However, these stimuli induced only minimal expression of VCAM-1 and E-selectinon HGF.Finally, binding assays using HGF and Molt4 cells showed induced these molecules to be functional, and the increased binding was blocked by a combination of mAb against ICAM-1 and leukocyte function-associated molecule-1 (LFA-1). Thus, the overexpression of ICAM-1 on gingival fibroblasts induced by cytokines and periodontopathic bacteria is speculated to be deeply involved in the retention and activation of LFA-1 bearing leukocytes in inflamed gingiva.
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Report
(3 results)
Research Products
(14 results)