| Project/Area Number |
62570570
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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 |
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Principal Investigator |
ONO Hitoshi (1988) Ehime University Assistant, 医学部附属病院, 助手 (80152536)
酒井 堅 (1987) 愛媛大学, 医学部・附属病院, 助手 (90136341)
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| Co-Investigator(Kenkyū-buntansha) |
佐川 庸 愛媛大学, 医学部附属病院, 助手
KUBO Meguru Ehime University Assistant, 医学部附属病院, 助手 (70186443)
NAKAGAWA Hironori Ehime University Assistant, 医学部附属病院, 助手 (80167543)
SAKAI Ken Ehime University Assistant, 医学部附属病院, 助手(元研究代表者) (90136341)
SAGAWA Teiri Ehime University Assistant
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Endotoxin shock / Lipopolysaccharide / Monoclonal antibody / Immunotherapy / Tumor necrosis factor / Interleukin-1 / Prostaglandin E_2 / エンドトキシン血症 / 受動免疫 / tumor necrosis factor / interleukin-1 / prostaglandinE_2 / エンドトキシン / O特異多糖 / Rコア多糖 / リピドA |
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| Research Abstract |
To study the efficacies of immunotherapy and the immunological mechanism involved in protection against bacterial endotoxemia, murine monoclonal antibodies (mAbs) against different determinants of lipopolysaccharide (LPS) were prepared. Anti-O polysaccharide mAb (igG3) reacted only with homologous LPS in ELISA. Anti-R core mAb (igG1) was crossreactive to various LPSs except for LPS derived from K.pneumoniae. Anti-Lipid A mAb (igG3) cross-reacted to all LPSs examined.
1. Prophylactic administration of homologous anti-O and anti-R mAbs suppressed the second fever onset in rabbits and reduced the mortality by endotoxin shock in galactosamine sensitized mice. 2. In parallel with the protectivity was the inhibitory capacity of mAbs in vitro to LPS-induced TNF production in BCG-activated macrophages. 3. However, both anti-O and anti-R mAbs markedly enhanced the LPS-induced iL-1 production by resident macrophages and exhibited opposite effects on PGE_2 production by these cells. Whereas the anti-O mAb was inhibitory, the anti-R mAb accelerated the PGE_2 production by LPS-stimulated cells. 4. The Anti-Lipid A mAb did not exhibit any effect on biological activities of LPS.
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