Cellular and molecular basis of the increased splenic hemopoiesis in mice treated with bacterial cell wall components.
Cellular and molecular basis of the increased splenic hemopoiesis in mice treated with bacterial cell wall components.
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用细菌细胞壁成分处理的小鼠脾脏造血增加的细胞和分子基础。
DOI：
10.1073/pnas.77.7.4322
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发表时间：
1980
影响因子：
11.1
通讯作者：
Metcalf,D
中科院分区：
文献类型：
--
作者：
Staber,FG;Metcalf,D
本文分析了注射细菌细胞壁成分类脂A和外膜脂蛋白后小鼠脾造血增加的机制。没有证据表明造血前体细胞上存在功能性脂质A受体。来自注射脂质A的小鼠的血清，在注射到正常小鼠中时，诱导脾脏中所有造血祖细胞的含量增加。反应的大小取决于使用的脂质A的剂量和转移到受体的血清的体积。当注射活性脂质A后血清时，对脂质A无反应的C3 H/HeJ小鼠表现出相似的脾脏变化。所有造血谱系的祖细胞，包括多潜能造血干细胞，参与了反应。结果表明，体液因子介导的脂质A诱导的脾造血增加。
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.