SHARED ACTIONS OF ENDOTOXIN AND TAXOL ON TNF RECEPTORS AND TNF RELEASE
SHARED ACTIONS OF ENDOTOXIN AND TAXOL ON TNF RECEPTORS AND TNF RELEASE
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DOI：
10.1126/science.1970196
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发表时间：
1990-04-20
期刊：
影响因子：
56.9
通讯作者：
NATHAN, CF
中科院分区：
文献类型：
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作者：
DING, AH;PORTEU, F;NATHAN, CF
细菌脂多糖(LPS)通过诱导巨噬细胞释放肿瘤坏死因子-α对哺乳动物宿主产生深远影响。(肿瘤坏死因子-α)；涉及的机制尚未解决。微管稳定剂紫杉醇分享了内毒素对巨噬细胞的两种作用：迅速降低肿瘤坏死因子-α。受体和触发的肿瘤坏死因子-α。放手。在低反应性C3H/HeJ小鼠中，紫杉醇的这两种作用均不存在。在重组近交系小鼠中，控制对脂多糖和紫杉醇反应的基因紧密相连。地塞米松可阻断肿瘤坏死因子-α的释放。但不能阻断肿瘤坏死因子-α的降低。感受器。因此，一种与微管相关的蛋白质可能是内毒素的细胞靶标。
Bacterial lipopolysaccharide (LPS) exerts profound effects on mammalian hosts in part by inducing macrophages to release tumor necrosis factor-.alpha. (TNF-.alpha.); the mechanism involved are unresolved. The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-.alpha. receptors and triggered TNF-.alpha. release. Both actions of taxol were absent in LPS-hyporesponsive C3H/HeJ mice. In recombinant inbred mice, the genes controlling responses to LPS and to taxol were closely linked. Dexamethasone blocked release of TNF-.alpha. by both stimuli but did not block the decrease in TNF-.alpha. receptors. Thus, a protein associated with microtubules may be a cellular target of LPS.