Mortensen R F
Exp Hematol. 1983 Sep;11(8):730-7.
Human C-reactive protein (CRP), an acute phase reactant purified from ascites fluids, selectively inhibited in vitro monocyte colony formation by bone marrow granulocyte-monocyte colony-forming cells (GM-CFC) from untreated mice, but not from mice that had undergone an acute systemic inflammatory response of 3-4 days duration. The CRP-susceptible M-CFC accumulated in the peritoneal cavity during the course of an inflammatory stimulus at this site. Aggregated CRP and CRP-complexes were as inhibitory as the monomeric form of purified CRP. Addition of phosphorylcholine (P-C), the major determinant on the C-polysaccharide (CPS) to which CRP binds, did not alter the inhibitory activity of CRP. Treatment of resident peritoneal macrophages with CRP did not lower their ability to serve as a source of CSF for GM-CFC. The results are consistent with a regulatory role for CRP during monocytopoiesis induced by inflammation.
人C反应蛋白(CRP)是一种从腹水液中纯化得到的急性期反应物,它能选择性地在体外抑制未处理小鼠骨髓粒细胞-单核细胞集落形成细胞(GM-CFC)形成单核细胞集落,但对经历了持续3-4天急性全身炎症反应的小鼠的GM-CFC没有抑制作用。在该部位的炎症刺激过程中,对CRP敏感的M-CFC积聚在腹腔中。聚合的CRP和CRP复合物与纯化的单体CRP一样具有抑制作用。添加CRP所结合的C多糖(CPS)上的主要决定因素磷酸胆碱(P-C),并不会改变CRP的抑制活性。用CRP处理腹腔常驻巨噬细胞,不会降低它们作为GM-CFC的CSF来源的能力。这些结果与CRP在炎症诱导的单核细胞生成过程中的调节作用一致。