Simms H H, Gaither T A, Fries L F, Frank M M
Department of Surgery, Rhode Island Hospital, Providence 02903.
J Immunol. 1991 Jul 1;147(1):265-72.
Freshly explanted monocytes phagocytosing IgG antibody-coated erythrocyte targets (EIgG) release a factor(s) that stimulates phagocytosis by neighboring monocytes and polymorphonuclear leukocytes (PMN). Culture supernatants obtained after 30-min incubation of adherent monocytes with EIgG, but not unopsonized sheep erythrocytes, markedly up-regulated the extent of PMN phagocytosis and enhanced the rate at which monocytes ingested EIgG. The presence of this factor(s) was first evident in phagocytic studies in which monocytes were prepared by a colloidal silica-based continuous gradient technique (Sepracell-Mn). After introduction of erythrocyte targets, there was a 20- to 30-min delay before initiation of phagocytosis that was not observed with monocytes prepared by the standard Percoll-gradient technique. Experiments suggest that, when compared with monocytes prepared by the Percoll-gradient method, Sepracell-Mn monocytes are closer to a base line state of activation with regard to the expression of Fc gamma RI and the ability to ingest EIgG. The mechanism of PMN upregulation by the monocyte factor(s) was explored. Monocyte supernatants did not induce an increase in the surface expression of PMN Fc gamma RI, II, or III. Neither anti-TNF, anti-IL-2, nor anti-GM-CSF had any significant effect on monocyte supernatant activity. Neutrophil activating protein-1 was not detected by ELISA. In contrast, anti-IL-1 completely blocked the effect of the supernatant on subsequent monocyte phagocytosis, and partially inhibited its effect on PMN phagocytosis. Furthermore, it was shown that RIL-1 as well as TNF markedly enhanced monocyte and PMN ingestion of EIgG. These results suggest that monocytes, after Fc gamma R-mediated phagocytosis, release monokines, including at least IL-1, which enhance the phagocytic function of neighboring PMN and monocytes to augment the host defense process.
刚分离出的吞噬IgG抗体包被红细胞靶标（EIgG）的单核细胞释放一种因子，可刺激相邻单核细胞和多形核白细胞（PMN）的吞噬作用。用EIgG孵育贴壁单核细胞30分钟后获得的培养上清液，而非未调理的绵羊红细胞，显著上调了PMN的吞噬程度，并提高了单核细胞摄取EIgG的速率。这种因子的存在首先在吞噬研究中得以显现，其中单核细胞是通过基于胶体二氧化硅的连续梯度技术（Sepracell-Mn）制备的。引入红细胞靶标后，吞噬作用开始前有20至30分钟的延迟，而用标准Percoll梯度技术制备的单核细胞则未观察到这种延迟。实验表明，与通过Percoll梯度法制备的单核细胞相比，Sepracell-Mn单核细胞在FcγRI的表达和摄取EIgG的能力方面更接近激活的基线状态。对单核细胞因子上调PMN的机制进行了探索。单核细胞上清液未诱导PMN FcγRI、II或III的表面表达增加。抗TNF、抗IL-2和抗GM-CSF对单核细胞上清液活性均无显著影响。通过ELISA未检测到中性粒细胞激活蛋白-1。相反，抗IL-1完全阻断了上清液对后续单核细胞吞噬作用的影响，并部分抑制了其对PMN吞噬作用的影响。此外，研究表明IL-1以及TNF显著增强了单核细胞和PMN对EIgG的摄取。这些结果表明，单核细胞在FcγR介导的吞噬作用后释放单核因子，至少包括IL-1，其增强相邻PMN和单核细胞的吞噬功能，以增强宿主防御过程。
