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衰老加速(SAM)小鼠骨髓对脂多糖反应的年龄相关性变化。

Age-related changes in myelopoietic response to lipopolysaccharide in senescence-accelerated (SAM) mice.

作者信息

Kumagai T, Morimoto K, Saitoh T, Tsuboi I, Aikawa S, Horie T

机构信息

First Department of Internal Medicine, Faculty of Medicine, Nihon University, Tokyo, Japan.

出版信息

Mech Ageing Dev. 2000 Jan 3;112(2):153-67. doi: 10.1016/s0047-6374(99)00085-8.

DOI:10.1016/s0047-6374(99)00085-8
PMID:10690927
Abstract

The effects of in vivo lipopolysaccharide (LPS) administration on myelopoiesis were examined in senescence-accelerated (SAM) mice. Young mice injected with LPS exhibited: (a) increased femoral proliferative pool size; (b) transient reduction in femoral non-proliferative pool size and number of femoral colony forming unit-granulocyte macrophages (CFU-GMs); (c) marked increase in splenic CFU-GMs; and (d) transient increase in S-phase of femoral CFU-GMs. The responses of old mice after LPS administration differed from those of young mice in the following points: (a) no recovery of the femoral non-proliferative pool or femoral CFU-GMs, (b) less significant augmentation of the femoral proliferative pool and splenic CFU-GMs, and (c) prolonged reduction in S-phase of femoral CFU-GM. Injection of LPS into mice resulted in a hyperproduction of colony-stimulating activity (CSA) in bone followed by production of colony-inhibitory activity (CIA) in young mice and in contrast, an excessive CIA secretion from bone without an increase in CSA levels in old mice. These imbalances in the regulatory factors derived from non-hemopoietic cells in the bones may lead to an inappropriate response of myelopoiesis in aged SAM mice after LPS administration, which may play a key role in infections.

摘要

在加速衰老(SAM)小鼠中检测了体内注射脂多糖(LPS)对骨髓生成的影响。注射LPS的年轻小鼠表现出:(a)股骨增殖池大小增加;(b)股骨非增殖池大小和股骨集落形成单位-粒细胞巨噬细胞(CFU-GM)数量短暂减少;(c)脾脏CFU-GM显著增加;(d)股骨CFU-GM的S期短暂增加。LPS给药后老年小鼠的反应在以下方面与年轻小鼠不同:(a)股骨非增殖池或股骨CFU-GM未恢复,(b)股骨增殖池和脾脏CFU-GM的增加不明显,(c)股骨CFU-GM的S期持续减少。给小鼠注射LPS会导致年轻小鼠骨骼中集落刺激活性(CSA)过度产生,随后产生集落抑制活性(CIA),相反,老年小鼠骨骼中CIA分泌过多而CSA水平没有增加。骨骼中非造血细胞衍生的调节因子的这些失衡可能导致老年SAM小鼠在LPS给药后骨髓生成的不适当反应,这可能在感染中起关键作用。

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引用本文的文献

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