1999 Fiscal Year Final Research Report Summary
Possible Role of Gingival Epithelial Cells in Host Defense Mechanism of Periodontal Disease Progression
| Project/Area Number |
10671971
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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 |
Periodontal dentistry
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| Research Institution | Kagoshima University |
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Principal Investigator |
IZUMI Yuichi Kagoshima University, Faculty of Dentistry, Professor, 歯学部, 教授 (60159803)
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| Co-Investigator(Kenkyū-buntansha) |
MINAMI Mutsumi Kagoshima University, Dental Hospital, Research Associate, 歯学部・附属病院, 助手 (60229771)
MATSUYAMA Takashi Kagoshima University, Faculty of Dentistry, Research Associate, 歯学部, 助手 (40253900)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Periodontal disease / Gingival epithelial cells / Gingival crevicular fluid / Host defence mechanism / SLPI / IL-1 / IL-1ra |
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| Research Abstract |
The purpose of the present research project was to detect the expression of secretory leukocyte protease inhibitor (SLPI) and IL-1 receptor antagonist (IL-1ra) in gingival epithelial cells and to clarify the possible relationship between SLPI in gingival crevicular fluid (GCF) and the periodontal clinical parameters.
SLPI was immunocytochemically detected on frozen-sectioned gingival epithelium and expressed on the surface and inside of cultured gingival keratinocytes from healthy gingiva. The levels of SLPI and α1-protease inhibitor (α1-PI) and neutrophil elastase (NE) activity in GCF were measured and periodontal clinical parameters were examined in fifteen adult periodontitis patients. In thirty examined sites, significantly higher amounts of SLPI, α1-PI, NE and GCF were consistently obtained in samples from periodontitis sites than in samples from healthy sites. SLPI, α1-PI and NE were found to correlate with probing depth. NE andα1-PI were significantly correlated with increasing c
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linical attachment loss. These results suggested that SLPI andα1-PI may be related to the inflammation in periodontitis sites.
To clarify the expression of IL-1 and IL-1ra in human gingival keratinocytes, we studied the protein production and mRNA expression of IL-1α and IL-1ra in human cultured gingival keratinocytes using enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction (RT-PCR). Furthermore, we studied immunohistochemically the presence of IL-1αand IL-1ra in the epithelium of healthy and inflamed gingiva. The level of cell-associated IL-1α was significantly increased under stimulation of TNF-α, while the level of IL- 1α in conditioned medium and the levels of IL-1ra protein were not influenced by TNF-α. IL-1α and intracellular IL-1ra mRNA transcripts were enhanced under stimulation with TNF-αby RT-PCR. Furthermore, the presence of IL-1ra, but not IL-1α, found by immunohistochemistry in the epithelium of gingiva. These results indicated that human gingival keratinocytes expressed IL-1αand IL-1ra, and may be involved in the regulation of inflammation of periodontal disease by IL-1αand IL-1ra. Less
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