Ageing mechanisms of hemopoietic system in senescence accelerated (SAM-P) mice.

衰老加速（SAM-p）小鼠外周血细胞数量随着年龄的增长而显著减少。该品系幼龄小鼠与老年小鼠相互骨髓移植发现，老年小鼠脾的分化支持功能较年轻小鼠弱。为了阐明老年小鼠造血微环境可能减少细胞因子的产生，我们测定了年轻和老年SAM-P小鼠粒细胞-巨噬细胞集落刺激因子（GM-CSF）的产生。与年轻小鼠相比，年老小鼠产生的GM-CSF要少得多。IL-E刺激可以诱导小鼠骨髓细胞产生GM-CSF，对IL-E刺激的反应程度在年轻小鼠和年老小鼠之间没有差异，尽管在这种情况下，老年小鼠的GM-CSF总量也比年轻小鼠少。在年轻和年老小鼠之间，白细胞介素-6的产生水平没有差异。这些结果表明，年龄相关的细胞因子产生减少是老龄SAM-P小鼠外周血细胞产生减少的原因。

Senescence accelerated (SAM-p) mice show a significant decrease in the number of peripheral blood cells with age. Mutual bone marrow transplantation between young and old mice of this strain revealed that the differentiation-supporting function of the spleen of the old mice was less active than that in the young mice.To elucidate the possible decrease in cytokine production by the hemopoietic microenvironmet of the old mice, we have assayd the production of granulocyte-macrophage colony stimulating factor (GM-CSF) in the young and old SAM-P mice.Old mice produced much less GM-CSF compared to young mice. Degree of the response to IL-E stimulation, which is known to induce GM-CSF production by the murine bone marrow cells, was not different between young and old mice, although the total amount of GM-CSF was less in the old mice than that in the young mice in this case, as well.There was no difference in the level of interleukin-6 production between young and old mice.These results suggest that age-related decrease in cytokine production is responsible for the decreased production of peripheral blood cells in the old SAM-P mice.