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Experimental elimination of tumor necrosis factor in low-dose endotoxin models has variable effects on survival.

机译:在低剂量内毒素模型中实验性消除肿瘤坏死因子对存活率具有可变影响。

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Tumor necrosis factor alpha (TNF) is thought to play a major role in the pathogenesis of septic shock. Anti-TNF antibody was preadministered in low-dose endotoxin lethality models in which BALB/c mice were challenged with small amounts of lipopolysaccharide following their sensitization with either carrageenan (CAR) or D-galactosamine (D-GalN). Although the antibody virtually eliminated circulating TNF in both the CAR and the D-GalN models, only the D-GalN model mice were afforded survival, adding to a growing body of evidence that substances other than TNF play a key role in endotoxin-induced lethality. Further examination of sera from these mice showed a much greater elevation of interleukin-6 levels in the CAR-sensitized group than in the D-GalN-sensitized group.
机译:肿瘤坏死因子α(TNF)被认为在败血性休克的发病机理中起主要作用。在低剂量内毒素致死性模型中预先给予抗TNF抗体,在该模型中,用角叉菜胶(CAR)或D-半乳糖胺(D-GalN)致敏后,BALB / c小鼠受到少量脂多糖的攻击。尽管该抗体实际上消除了CAR和D-GalN模型中的循环TNF,但只有D-GalN模型小鼠可以存活,这增加了越来越多的证据表明,除TNF以外的其他物质在内毒素致死性中起关键作用。这些小鼠的血清进一步检查显示,与D-GalN致敏组相比,CAR致敏组的白细胞介素6水平升高得多。

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