Rampart M, Fiers W, de Smet W, Herman A G
Department of Experimental Pharmacology, University of Antwerp, Belgium.
Agents Actions. 1989 Jan;26(1-2):186-8. doi: 10.1007/BF02126603.
The pro-inflammatory properties of IL 1 and TNF were investigated in an in vivo model of inflammation. IL 1 induced PMN leukocyte accumulation that was slow in onset, reaching a peak rate at 3-4 h and that was inhibitable by Actinomycin D and Cycloheximide. PMN leukocyte emigration was not associated with any significant plasma leakage. In contrast, TNF induced PMN leukocyte accumulation and oedema formation, that were rapid in onset and very short of duration (t1/2 6-10 min). TNF-induced plasma leakage was PMN leukocyte-, but not protein biosynthesis-dependent. The differences in time course and biological profile suggest that IL 1 and TNF exert their pro-inflammatory effects in vivo via different mechanisms.
在炎症的体内模型中研究了白细胞介素1(IL 1)和肿瘤坏死因子(TNF)的促炎特性。IL 1诱导多形核白细胞(PMN)积聚,其起效缓慢,在3 - 4小时达到峰值速率,并且可被放线菌素D和环己酰亚胺抑制。PMN白细胞迁移与任何明显的血浆渗漏无关。相比之下,TNF诱导PMN白细胞积聚和水肿形成,其起效迅速且持续时间非常短(半衰期6 - 10分钟)。TNF诱导的血浆渗漏依赖于PMN白细胞,但不依赖于蛋白质生物合成。时间进程和生物学特征的差异表明,IL 1和TNF在体内通过不同机制发挥其促炎作用。