Chen B D, Lin H S, Hsu S
J Immunol. 1983 May;130(5):2256-60.
These studies demonstrate the potent effect of bacterial endotoxin (LPS) on the inhibition of iodinated colony-stimulating factor- (125I-CSF-1) binding by murine peritoneal exudate macrophages (PEM) from C3H/An and C57BL/6 mice. As small an amount as 0.1 ng/ml LPS is sufficient to cause a significant inhibitory effect; this effect is temperature-, time- and concentration-dependent. LPS, however, causes minimal or no inhibition of 125I-CSF-1-binding by PEM from LPS-resistant C3H/HeJ mice. Inhibition of 125I-CSF-1-binding does not appear to be a result of a direct occupancy by LPS of CSF-1 receptors present on the cell membrane and is most likely due to a progressive loss of available CSF-1-binding sites. The effect can be neutralized by the addition of the antibiotic polymyxin B, which binds to the lipid A portion of LPS. The action of LPS on PEM is transient; treated cells recover their 125I-CSF-1-binding activity whether or not LPS is later removed. The restoration of 125I-CSF-1-binding activity can be blocked completely by the addition of cyclohexamide. These findings suggest the rapid, LPS-induced disappearance of CSF-1 receptors from the cell surface may be related to the activation of macrophages by LPS.
这些研究证明了细菌内毒素（LPS）对来自C3H/An和C57BL/6小鼠的鼠腹膜渗出巨噬细胞（PEM）抑制碘化集落刺激因子-（125I-CSF-1）结合的强大作用。低至0.1 ng/ml的LPS就足以产生显著的抑制作用；这种作用是温度、时间和浓度依赖性的。然而，LPS对来自LPS抗性C3H/HeJ小鼠的PEM的125I-CSF-1结合产生的抑制作用最小或没有抑制作用。125I-CSF-1结合的抑制似乎不是由于LPS直接占据细胞膜上存在的CSF-1受体，最可能是由于可用的CSF-1结合位点逐渐丧失。通过添加与LPS的脂质A部分结合的抗生素多粘菌素B，可以中和这种作用。LPS对PEM的作用是短暂的；无论LPS后来是否被去除，处理过的细胞都能恢复其125I-CSF-1结合活性。添加环己酰胺可以完全阻断125I-CSF-1结合活性的恢复。这些发现表明，LPS诱导的CSF-1受体从细胞表面快速消失可能与LPS激活巨噬细胞有关。
