| Project/Area Number |
06671210
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Ehime University School of Medicine |
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Principal Investigator |
OSUKA Yo Ehime University School of Medicine. Assistant professor, 医学部, 教授 (10036486)
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| Co-Investigator(Kenkyū-buntansha) |
NAKATA Tetsuhiro Ehime University School of Medicine. Assistant, 医学部・附属病院, 助手 (40260690)
ABE Yasuhito Ehime University School of Medicine. Assistant, 医学部, 助手 (30184229)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | TNF / lymphotoxin / TNF receptor / neutrophils / 腫瘍壊死因子レセプター / 生物活性 |
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| Research Abstract |
The expression and biological role of 55- and 75-kDa tumor necrosis factor-receptors (TNF-R) in human polymorphonuclear cells (PMN) in vitro were studied using agonistic rabbit polyclonal anti-TNF-R antibodies. PMN express 75-kDa TNF-R predominantly according to flow cytometric analysis and a ^<125>I-LT binding assay. PMN produce and release the superoxide anion on stimulation by human recombinant lymphotoxin (LT) in vitro. Anti-55- but not anti-75-kDa TNF-R antibody stimulated the superoxide release mimicking LT.Release of the elastase from azurophilic granule of PMN was augmented by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody augmented the clastase release mimicking LT.Release of the lactoferrin from the specific granules of PMN was enhanced by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody enhanced the laccoferrin release. These antibodies failed to co-stimulate these PMN functions. The peak adhesiveness of PMN to a plastic plate and the peak expression of Mac-1 adhesion molecule (CD11b/CD18) on PMN were upregulated by LT in vitro. Anti-55- but not anti-75-kDa TNF-R antibody upregulated the peak adhesiveness of PMN and CD11b/CD18 expression mimicking LT.Though anti-75-kDa TNF-R antibody by itself did not alter the adhesiveness and marginally suppressed Mac-1 expression of PMN,it maintained the adhesiveness and adhesion molecule expression in the presence of anti-55-kDa TNF-R antibody. In summary, PMN predominantly express 75-kDa TNF-R,the signaling of LT (and TNF) in PMN is mediated mainly by 55-kDa TNF-R,and the adhesion function can be modulated also by 75-kDa TNF-R when 55-kDa TNF-R is stimulated.
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