2001 Fiscal Year Final Research Report Summary
MECHANISM OF PROLONGED INFLAMMATION IN THE ORAL:EFFECT OF NEUTROPHIL APOPTOSIS ON ENDOTHELIAI CELLS
| Project/Area Number |
12671962
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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 |
Surgical dentistry
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| Research Institution | SHOWA UNIVERSITY |
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Principal Investigator |
IWASE Masayasu SHOWA UNIV SCHOOL OF DENTISTRY, ASSISTANT PROFFESOR, 歯学部, 講師 (50193743)
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| Co-Investigator(Kenkyū-buntansha) |
OHASHI Masaru SHOWA UNIVERSITY SCHOOL OF DENTISTRY, ASSISTANT, 歯学部, 助手 (40317524)
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| Project Period (FY) |
2000 – 2001
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| Keywords | APOPTOSIS / FAS / NEUTROPHILS / ENDOTHELIAL CELLS / ADOHESIVEMOLECULE / CYTOKINE / CHEMOKINE / NSAID |
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| Research Abstract |
1) Endothelial cells, HUVECs, constitutively expressed Fas antigen on cell surface.
2) HUVECs were induced apoptosis by the addition of anti-Fas, CH-11.
3) When HUVECs and neutrophils were co cultured in the presence of anti-Fas, they lost adhesive function each other.
4) When neutrophils were treated with anti-Fas, the expressions of CD11b and CD18 decreased in its cell surface. Therefore, adhesive dysfunction was dependent on adhesive molecule on neutrophils.
5) Because chemokine and inflammatory cytokine reduced Fas-mediated apoptosis on HUVECs and neutrophils, these agents maintained neutrophil function in the acute inflammatory tissues.
6) In contrast, NSAIDs enhanced Fas-mediated apoptosis on HUVECs and neutrophils, then this event was new a strategy for anti-infiammatory function of NSAIDs.
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Research Products
(11 results)
