Le Contel C, Vinit M A, Parant F J, Parant M A
Laboratory of Immunopharmacology, Institut Biomédical des Cordeliers, Paris, France.
Cytokine. 1990 Sep;2(5):375-80. doi: 10.1016/1043-4666(90)90068-5.
In unprimed mice, a single injection of a non-lethal dose of lipopolysaccharide (LPS) produced a rise in tumor necrosis factor (TNF) and interleukin 6 (IL 6) activities. Peak serum concentrations were attained, respectively, 1.5 hr and 2.5 hr after the challenge. Pretreatment with recombinant human TNF-alpha (rHuTNF) had a priming effect for enhanced production of both serum cytokines without any change in kinetics. The enhancement was more pronounced in the TNF (15-fold) than in the IL 6 (4-fold) response. Recombinant murine TNF caused a comparable increase in LPS-induced cytokine release. In contrast, comparable pretreatment with another macrophage-derived cytokine, recombinant human interleukin 1 beta (HuIL1-beta), revealed a negative effect on LPS-induced TNF release whereas IL 6 in the blood reached levels similar to those found after priming with rTNF. Moreover, when administered in combination with rHuTNF, rHuIL1-beta inhibited the priming effect on TNF autocrine production.
在未致敏的小鼠中，单次注射非致死剂量的脂多糖（LPS）会使肿瘤坏死因子（TNF）和白细胞介素6（IL-6）的活性升高。在注射刺激后分别于1.5小时和2.5小时达到血清峰值浓度。用重组人TNF-α（rHuTNF）进行预处理对增强两种血清细胞因子的产生具有致敏作用，动力学无任何变化。TNF的增强作用（15倍）比IL-6（4倍）更明显。重组鼠TNF在LPS诱导的细胞因子释放方面引起类似的增加。相反，用另一种巨噬细胞衍生的细胞因子重组人白细胞介素1β（HuIL1-β）进行类似的预处理，对LPS诱导的TNF释放显示出负面影响，而血液中的IL-6达到与用rTNF致敏后相似的水平。此外，当与rHuTNF联合给药时，rHuIL1-β抑制对TNF自分泌产生的致敏作用。
