1999 Fiscal Year Final Research Report Summary
Regulation of neutrophil apoptosis in periodontitis: possible involvement of Fas/FasL and Fas-dependent signaling pathway
| Project/Area Number |
09671962
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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 |
Conservative dentistry
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| Research Institution | Meikai University |
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Principal Investigator |
SHIINOJIMA Takahiro Meikai Univ. Sch. Of Dentistry, Lecturer, 歯学部, 講師 (60146230)
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| Co-Investigator(Kenkyū-buntansha) |
TATSUMI Junichi Meikai Univ. Sch. Of Dentistry, Lecturer, 歯学部, 講師 (60227105)
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| Project Period (FY) |
1997 – 1999
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| Keywords | Neutrophil / Apoptosis / Eas / FasL / sFas / sFasL / Lipopolysaccharide / Periodontal tissue destruction |
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| Research Abstract |
Many factors, such as cytokines and bacterial products, are known to affect the life span of PMNs. The author investigated whether P.gingivalis LPS retards the apoptotic process of PMNs and, if so, whether the delayed apoptosis is related to Fas, FasL, or soluble form of these molecules. During incubation in the regular culture medium, the viability of PMNs progressively declined, producing apoptotic cells, characterized by chromatin condensation, internucleosomal DNA fragmentation, cell shrinkage and blebbing of plasma membrane. P.gingivalis LPS significantly increased the viability of PMNs and reduced the production of fragmented DNA, as efficiently as E.coli LPS. Western blot analysis demonstrates that Fas expression was not changed but FasL expression slightly declined. sFas and sFasL expression were increased when PMNs were treated with LPS. Among five sFas variants, only Fas Exo6 Del was detectable. Fas mRNA expression was increased whereas there is little difference of FasL mRNA expression. The present study suggests that the retardation of PMNs apoptosis by P.gingivalis LPS may modulate the restoration of acute inflammation in the periodontal tissues, where activated PMNs accumulate. The delayed apoptosis can partly be explained by Fas/FasL system. The author propose here that this inhibition of PMNs apoptosis may be related to increased sFas(Fas Exo6 Del) and processing of membrane-bound FasL by LPS during early stage of apoptosis.
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