Armstrong J W, Kirby-Dobbels K, Chapes S K
Division of Biology, Kansas State University, Manhattan 66506, USA.
J Appl Physiol (1985). 1995 Mar;78(3):968-75. doi: 10.1152/jappl.1995.78.3.968.
Antiorthostatically suspended mice had suppressed macrophage development in both unloaded and loaded bones, indicating a systemic effect. Bone marrow cells from those mice secreted less macrophage colony-stimulating factor (M-CSF) and interleukin-6 (IL-6) than did control mice. Because M-CSF and IL-6 are important to bone marrow macrophage maturation, we formulated the hypothesis that suppressed macrophage development occurred as a result of the depressed levels of either M-CSF or IL-6. To test the hypothesis, mice were administered recombinant M-CSF or IL-6 intraperitoneally. We showed that recombinant M-CSF therapy, but not recombinant IL-6 therapy, reversed the suppressive effects of antiorthostatic suspension on macrophage development. These data suggest that bone marrow cells that produce M-CSF are affected by antiorthostatic suspension and may contribute to the inhibited maturation of bone marrow macrophage progenitors.
抗直立位悬吊小鼠在失重和负重骨骼中均出现巨噬细胞发育受抑制的情况,表明存在全身效应。这些小鼠的骨髓细胞分泌的巨噬细胞集落刺激因子(M-CSF)和白细胞介素-6(IL-6)比对照小鼠少。由于M-CSF和IL-6对骨髓巨噬细胞成熟很重要,我们提出假说,即巨噬细胞发育受抑制是由于M-CSF或IL-6水平降低所致。为验证该假说,给小鼠腹腔注射重组M-CSF或IL-6。我们发现,重组M-CSF治疗可逆转抗直立位悬吊对巨噬细胞发育的抑制作用,而重组IL-6治疗则不能。这些数据表明,产生M-CSF的骨髓细胞受抗直立位悬吊影响,可能导致骨髓巨噬细胞祖细胞成熟受抑制。