| 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)
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| 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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