Everaerdt B, Brouckaert P, Shaw A, Fiers W
Laboratory of Molecular Biology, State University, Gent, Belgium.
Biochem Biophys Res Commun. 1989 Aug 30;163(1):378-85. doi: 10.1016/0006-291x(89)92146-3.
We studied the induction of lethal shock by Tumour Necrosis Factor (TNF) in mice and observed a remarkable difference between the effect of human and murine TNF, which could be eliminated by co-administration of sensitizing agents. We identified interleukin-1 (IL1) as a natural sensitizer, rendering mice as susceptible to human TNF as to murine TNF. This IL1 activity was found to be exerted to the same extent both by human and murine IL1-alpha or IL1-beta, and was also different from the sensitization obtained with galactosamine, since these agents had an additive effect. Pretreatment of the animals with indomethacin, a cyclooxygenase inhibitor, provided partial protection against TNF lethality in IL1-sensitized but not in galactosamine-sensitized mice.
我们研究了肿瘤坏死因子（TNF）在小鼠中诱导致死性休克的情况，并观察到人类和小鼠TNF的作用存在显著差异，而通过同时给予致敏剂可消除这种差异。我们确定白细胞介素-1（IL1）为天然致敏剂，使小鼠对人类TNF的敏感性与对小鼠TNF的敏感性相同。发现人类和小鼠的IL1-α或IL1-β发挥的这种IL1活性程度相同，并且也与用半乳糖胺获得的致敏作用不同，因为这些药物具有相加作用。用环氧化酶抑制剂吲哚美辛预处理动物，可对IL1致敏的小鼠提供部分保护以抵抗TNF致死性，但对半乳糖胺致敏的小鼠则无此作用。
