Staber F G, Metcalf D
Proc Natl Acad Sci U S A. 1980 Jul;77(7):4322-5. doi: 10.1073/pnas.77.7.4322.
An analysis was made of the mechanisms responsible for the increased splenic hemopoiesis occurring in mice after the injection of the bacterial cell wall components lipid A and outer membrane lipoprotein. No evidence was obtained for the presence of functional lipid A receptors on hemopoietic precursor cells. Serum from lipid A-injected mice, on injection into normal mice, induced in the spleen an increased content of all hemopoietic progenitor cells. The magnitude of the response was dependent on the dose of lipid A used and the volume of serum transferred to the recipients. C3H/HeJ mice unresponsive to lipid A exhibited similar spleen changes when injected with active post-lipid A sera. Progenitor cells of all hemopoietic lineages, including multipotential hemopoietic stem cells, were involved in the response. The results suggest that a humoral factor mediates the lipid A-induced increase of splenic hemopoiesis.
对注射细菌细胞壁成分脂多糖（lipid A）和外膜脂蛋白后小鼠脾脏造血增加的机制进行了分析。未获得造血前体细胞上存在功能性脂多糖受体的证据。将注射脂多糖的小鼠血清注入正常小鼠后，可诱导脾脏中所有造血祖细胞含量增加。反应的程度取决于所用脂多糖的剂量和转移至受体的血清体积。对脂多糖无反应的C3H/HeJ小鼠在注射活性脂多糖后血清时，脾脏也出现类似变化。包括多能造血干细胞在内的所有造血谱系的祖细胞均参与了该反应。结果表明，一种体液因子介导了脂多糖诱导的脾脏造血增加。
