1997 Fiscal Year Final Research Report Summary
Pothogenic mechanism of oral severe infection : Effect of oxidativc stress on neutrophil apoptosis.
| Project/Area Number |
08672333
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Showa University |
|---|
Principal Investigator |
IWASE Masayasu Showa University Sch of Dentistry, Assistant Prof, 歯学部, 講師 (50193743)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Masako Showa University Sch of Dentistry, Senior Fellow, 歯学部, 助手 (80286856)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Keywords | Neutrophil / Apoptosis / Fas antigen / Fas ligand / Auute inflammation / Differentiotion / Cytokine / Chemoattractant |
|---|
| Research Abstract |
1.Fas and Fas ligand were expressed on neutrophils consitutively. The expression of Fas increased in postsurgical acute inflammation, whereas the expression of Fas ligand on neutrophils was constant during observation. The levels of soluble Fas antigen in serum were also unchangeable postsurgically. Soluble Fas ligand levels were undetectable in any serum samples in this study.
2.A chemoattractant such as FMLP,PAF,LTB4 and IL-8 did not change the expression of Fas/Fas ligand of neutrophils. Apoptosis of neutrophils exhibited the increase/decrease by addition of the chemoattractants. GTP protein inhibitor and tyrosin kinase inhibitor reduced the mode.
3.The-expression of Fas antigen on HL-60 cells was increased with a differentiation inducing factor including DMSO,RA and 1,25 (OH)_2 VD_<3・> On the contrary, bcl-2 protein in HL-60 cells was decreased by treatment of the factor. These results suggest that differentiated HL-60 cells may become susceptible to Fas/Fas ligand mediated apoptosis.
4.The expression of Fas antigen on HL-60 cells was also increased with INF-gamma or TNF-alpha. These results indicate that cytokine such as INF-gamma or TNF-alpha regulates a susceptibility of Fas mediated cell death.
|
