Goto F, Goto K, Mori S, Ohkawara S, Yoshinaga M
Department of Pathology, Kumamoto University Medical School, Japan.
Br J Exp Pathol. 1989 Dec;70(6):597-606.
Biosynthesis of interleukin-I beta (IL-I beta) by inflammatory peritoneal exudate cells (PEC) was studied in terms of biological activity (thymocyte co-mitogenic assay), IL-I beta mRNA expression (cytoplasmic slot blot analysis) and detection of immunoreactive IL-I beta molecule (immunocytochemistry). Our findings were taken to conclude that IL-I beta expression was observed only in PEC harvested from early inflammatory site and the kinetic profile of the IL-I activity during the course of the inflammation was explained by IL-I beta mRNA expression, namely de-novo synthesis by inflammatory exudate cells. With respect to a single cell level, it was definitely proved that polymorphonuclear leucocytes were the major producer of IL-I beta during the casein-induced acute inflammation in rabbits.
通过生物活性（胸腺细胞共刺激测定）、白细胞介素-1β（IL-1β）mRNA表达（细胞质狭缝印迹分析）和免疫反应性IL-1β分子检测（免疫细胞化学），研究了炎性腹膜渗出细胞（PEC）对IL-1β的生物合成。我们的研究结果得出结论，仅在从早期炎症部位收集的PEC中观察到IL-1β表达，并且炎症过程中IL-1活性的动力学特征可以通过IL-1βmRNA表达来解释，即炎性渗出细胞的从头合成。就单细胞水平而言，明确证明了在兔酪蛋白诱导的急性炎症过程中，多形核白细胞是IL-1β的主要产生者。
