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Burn Wound Infection-Induced Myeloid SuppressionThe Role of Prostaglandin E sub 2, Elev...
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Burn Wound Infection-Induced Myeloid SuppressionThe Role of Prostaglandin E sub 2, Elevated Adenylate Cyclase, and Cyclic Adenosine Monophosphate
作者:
Richard L. Gamelli,
Li-Ke He,
Hong Liu,
John D. Ricken,
期刊:
The Journal of Trauma: Injury, Infection, and Critical Care
(OVID Available online 1998)
卷期:
Volume 44,
issue 3
页码: 469-474
ISSN:0022-5282
年代: 1998
出版商: OVID
数据来源: OVID
摘要:
Suppressed granulocyte and macrophage growth after burn infection or endotoxicosis appears to be mediated by macrophage-derived products. In this study, we found that after burn, burn plus infection, or endotoxicosis, peritoneal-elicited macrophages or bone marrow cells released increased amounts of prostaglandin E2(PGE2) and inhibited growth of granulocyte-macrophage progenitor cells (GM-CFC). PGE sub 2, when added in culture, inhibited in vitro GM-CFC growth in a dose-dependent manner. Pretreatment of bone marrow cells with either dibutyryl cyclic adenosine monophosphate or Forskolin in vitro mimicked the PGE2inhibition, further aggravated the inhibition induced by burn, burn plus infection, or endotoxicosis, and was not blocked by co-culture with indomethacin. Pretreatment of bone marrow cells with SQ22536, an adenylate cyclase inhibitor, significantly restored the suppressed GM-CFC growth found after burn, burn plus infection, or endotoxicosis. Alterations in myeloid production after burn infection appear to be related in part to the level of intracellular cyclic adenosine monophosphate for the GM-CFC and are responsive to PGE2.
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