Commins L M, Loegering D J, Minnear F L
Department of Physiology, Albany Medical College, New York 12208.
Circ Shock. 1989 Mar;27(3):237-44.
Depression of Kupffer cell complement receptor (CR) function is associated with several states of depressed host defense. This study was carried out to determine if ibuprofen and dexamethasone, which decrease the mortality rate following endotoxemia, could prevent the depression of CR function caused by endotoxemia and the phagocytosis of antibody-coated erythrocytes (EIgG). The depression of CR function caused by endotoxin was completely prevented by the administration of ibuprofen or dexamethasone. Thus, the ability of these drugs to prevent the depression of macrophage function may contribute to their salutory effects during endotoxin shock. In contrast to the effect with endotoxemia, the depression of CR function caused by the phagocytosis of EIgG was not modified by pretreatment with ibuprofen or dexamethasone. Additional studies demonstrated that the depression of CR function caused by EIgG was probably not due to EIgG in the blood or bound to Kupffer cells, interfering with the receptor probe for access to the CR. This study has shown that ibuprofen and dexamethasone can prevent the depression of CR function caused by endotoxin but not the depression caused by the phagocytosis of EIgG. These results suggest that different mechanisms mediate the depression of CR function caused by endotoxin and the phagocytosis of EIgG.
库普弗细胞补体受体（CR）功能的抑制与宿主防御功能降低的几种状态相关。本研究旨在确定可降低内毒素血症后死亡率的布洛芬和地塞米松是否能预防内毒素血症及抗体包被红细胞（EIgG）吞噬作用所导致的CR功能抑制。给予布洛芬或地塞米松可完全预防内毒素所致的CR功能抑制。因此，这些药物预防巨噬细胞功能抑制的能力可能有助于其在内毒素休克期间发挥有益作用。与内毒素血症的作用相反，布洛芬或地塞米松预处理并未改变EIgG吞噬作用所导致的CR功能抑制。进一步研究表明，EIgG所致的CR功能抑制可能并非由于血液中或与库普弗细胞结合的EIgG干扰了受体探针与CR的结合。本研究表明，布洛芬和地塞米松可预防内毒素所致的CR功能抑制，但不能预防EIgG吞噬作用所致的抑制。这些结果提示，内毒素和EIgG吞噬作用导致CR功能抑制的机制不同。
