肿瘤坏死因子和血小板活化因子在黑猩猩内毒素诱导的单核细胞趋化蛋白1和巨噬细胞炎性蛋白1β释放中的不同作用
Divergent roles of tumor necrosis factor and platelet-activating factor in endotoxin-induced release of monocyte chemoattractant protein 1 and macrophage inflammatory protein 1beta in chimpanzees.
作者信息
Dekkers P E, Levi M, van Deventer S J, van der Poll T
机构信息
Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
出版信息
Infect Immun. 1999 Oct;67(10):5480-2. doi: 10.1128/IAI.67.10.5480-5482.1999.
Abstract
A platelet-activating factor receptor antagonist reduced the release of macrophage inflammatory protein 1beta (MIP-1beta) during endotoxemia in chimpanzees but did not influence the secretion of monocyte chemoattractant protein 1 (MCP-1). Anti-tumor necrosis factor alpha monoclonal antibody completely prevented MCP-1 release and simultaneously enhanced the secretion of MIP-1beta. Levels of MIP-1beta and MCP-1 release were differentially regulated during endotoxemia.
摘要
血小板激活因子受体拮抗剂可减少黑猩猩内毒素血症期间巨噬细胞炎性蛋白1β（MIP-1β）的释放，但不影响单核细胞趋化蛋白1（MCP-1）的分泌。抗肿瘤坏死因子α单克隆抗体可完全阻止MCP-1的释放，同时增强MIP-1β的分泌。内毒素血症期间，MIP-1β和MCP-1的释放水平受到不同的调节。
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