Udupa K B, Sharma B G
Education and Clinical Center, V.A. Medical Center, Little Rock, AR 72205, USA.
Am J Hematol. 1996 Jul;52(3):178-83. doi: 10.1002/(SICI)1096-8652(199607)52:3<178::AID-AJH7>3.0.CO;2-Q.
Injection of bacterial endotoxin or granulocyte/macrophage colony-stimulating factor (GM-CSF) into exhypoxic polycythemic mice simultaneously with erythropoietin (EPO) suppressed erythroid cell formation, as monitored by 59Fe incorporation into circulating red blood cells. This effect was dose-dependent and time-dependent. GM-CSF did not inhibit erythroid cell formation directly, as the antibody to the GM-CSF did not neutralize the effect of endotoxin, the inducer of GM-CSF. The suppression of both agents could be partially corrected by prior injection of a monoclonal antibody to tumor necrosis factor alpha (anti-TNF alpha). These results indicate that the suppression of EPO-induced erythroid cell formation by endotoxin and GM-CSF was due in part to the production of TNF alpha.
在内毒素或粒细胞/巨噬细胞集落刺激因子（GM-CSF）与促红细胞生成素（EPO）同时注射到低氧性红细胞增多症小鼠体内时，可抑制红系细胞生成，这通过将59Fe掺入循环红细胞中进行监测。这种效应呈剂量依赖性和时间依赖性。GM-CSF并不直接抑制红系细胞生成，因为抗GM-CSF抗体不能中和GM-CSF诱导剂内毒素的作用。预先注射肿瘤坏死因子α单克隆抗体（抗TNFα）可部分纠正这两种药物的抑制作用。这些结果表明，内毒素和GM-CSF对EPO诱导的红系细胞生成的抑制作用部分归因于TNFα的产生。
