Schade S G, Fried W
Am J Physiol. 1976 Jul;231(1):73-6. doi: 10.1152/ajplegacy.1976.231.1.73.
Infection may be associated with failure of erythropoiesis, and endotoxin has been shown to cause a decrease in the number of erythroid cells in the marrow of mice. We have investigated the effect of endotoxin on erythropoiesis in BDF1 mice by studying its effect on the incorporation of intravenously administered 59Fe into peripheral red cells. In normal mice the injection of endotoxin 2 and 3 days prior to the administration of 59Fe results in suppression of its incorporation into red cells. In exhypoxic polycythemic mice, endotoxin suppresses the response to erythropoietin injection when the endotoxin is given prior to or at the same time as the erythropoietin. This effect is much less marked when endotoxin is given after erythropoietin. We conclude that endotoxin either 1) impairs the function of erythropoietin-responsive cells, 2) competively decreases erythroid progenitors by stimulating granulocytes, or 3) inactivates erythropoietin.
感染可能与红细胞生成失败有关，并且内毒素已被证明可导致小鼠骨髓中红系细胞数量减少。我们通过研究内毒素对静脉注射的59Fe掺入外周红细胞的影响，来探讨其对BDF1小鼠红细胞生成的作用。在正常小鼠中，在给予59Fe前2天和3天注射内毒素会导致其掺入红细胞的过程受到抑制。在低氧性红细胞增多症小鼠中，当在内毒素与促红细胞生成素同时或在其之前给予时，内毒素会抑制对促红细胞生成素注射的反应。当在内毒素在促红细胞生成素之后给予时，这种作用则不太明显。我们得出结论，内毒素要么1）损害促红细胞生成素反应性细胞的功能，2）通过刺激粒细胞竞争性地减少红系祖细胞，要么3）使促红细胞生成素失活。
