1999 Fiscal Year Final Research Report Summary
Pathogenic mechanism of oral severe infection: Analysis of phagocytic process for apoptotic neutrophils
| Project/Area Number |
10671907
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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 University, School of Dentistry, Assistant Professor, 歯学部, 講師 (50193743)
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| Co-Investigator(Kenkyū-buntansha) |
TACHIBANA Hideharu Showa University, School of Dentistry, Senior Fellow, 歯学部, 助手 (70317577)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Apoptosis / Neutrophil / Fas / Caspase / Glutathione / Chemotactic factor / FLIP / Adhesion molecule |
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| Research Abstract |
1. Anti-Fas treated neutrophils were reduced cell attachment, because adhesion molecules of neutrophils were altered during apoptotic process; enhancement of CD11b, CD11c and CD18, reduction of CD11a, CD15 and CD62L, no change of CD31. The expression of adhesion molecules was affected by chemotactic factors such as FMLP, C5a, PAF, LTB4 and IL-8. Neutrophil apoptosis was enhanced by chemotactic factors without the expression of Fas.
2. Neutrophils on post-operative surgery day 1 were delayed Fas-mediated apoptosis accompanied with reduction of caspase-3 and -8 activities. Plasma factors on surgical-induced acute inflammation also inhibited apoptosis of neutrophils. Neutrophils on acute inflammation exhibited reduction of glutathione levels, but not alter expression of Fas and FLIP levels compared with resident neutrophils. Plasma on acute inflammation contained lots of glutathione and proinflammatory cytokines. Anti-proinflammatory cytokine decreased in inhibitory effect of plasma on apoptosis. Exogenous glutathione and NAC were also inhibited Fas-mediated apoptosis of neutrophils via upstream of caspase-8.
3. Differentiated HL-60 cells by DMSO or RA were enhanced Fas-mediated apoptosis because of reduction of glutathione and FLIP levels in cytoplasma and enhancement of expression of Fas in membrane.
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