van Waarde D, Hulsing-Hesselink E, van Furth R
Blood. 1977 Oct;50(4):727-42.
A factor increasing monocytopoiesis (FIM) has been demonstrated during the onset of an acute inflammatory reaction caused by an intraperitoneal injection of polystyrene latex particles. It is protein in nature, does not contain a carbohydrate moiety essential for its function, and is very probably not a glycoprotein. The molecular weight of FIM lies between 18,000 and 24,000 daltons (determined with both ultrafiltration membranes and gel filtration on Sephadex G100). The monocytosis induced by FIM is dose dependent. FIM is thermolabile, having a half-time of about 20 min at 37 degrees C in serum; temperature inactivation can be delayed by the addition of epsilon-aminocaproic acid, the half-time at 37 degrees C then being about 45 min. In vitro treatment of normal murine blood with the inducers of the inflammatory reaction does not result in FIM activity in the serum. FIM dose not have chemotactic activity toward macrophages, is not a clotting factor, is not a biologically active fragment of the complement system, and has no colony-stimulating or-enhancing activity in the vitro bone marrow colony assay. On the basis of these results, a mechanism is postulated for the humoral regulation of monocytopoiesis.
在腹腔注射聚苯乙烯乳胶颗粒引起的急性炎症反应开始期间，已证明存在一种增加单核细胞生成的因子（FIM）。它本质上是蛋白质，不包含其功能所必需的碳水化合物部分，很可能不是糖蛋白。FIM的分子量在18,000至24,000道尔顿之间（通过超滤膜和Sephadex G100凝胶过滤测定）。FIM诱导的单核细胞增多症具有剂量依赖性。FIM对热不稳定，在血清中37℃时半衰期约为20分钟；加入ε-氨基己酸可延迟温度失活，此时37℃时的半衰期约为45分钟。用炎症反应诱导剂对正常小鼠血液进行体外处理不会导致血清中出现FIM活性。FIM对巨噬细胞没有趋化活性，不是凝血因子，不是补体系统的生物活性片段，并且在体外骨髓集落测定中没有集落刺激或增强活性。基于这些结果，推测了一种单核细胞生成体液调节的机制。
