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骨骼失用会导致免疫细胞反应出现器官特异性变化。

Skeletal unloading causes organ-specific changes in immune cell responses.

作者信息

Armstrong J W, Nelson K A, Simske S J, Luttges M W, Iandolo J J, Chapes S K

机构信息

Division of Biology, Kansas State University, Manhattan 66506.

出版信息

J Appl Physiol (1985). 1993 Dec;75(6):2734-9. doi: 10.1152/jappl.1993.75.6.2734.

Abstract

The effects of skeletal unloading using antiorthostatic tail suspension on the mouse immune system are tissue specific. This phenomenon was demonstrated by analyzing cells from the lymph nodes, spleen, and bone marrow. Phytohemagglutinin-induced T-cell proliferation was depressed in lymph nodes after 11 days of antiorthostatic suspension. In contrast, splenic T-cell proliferation in response to phytohemagglutinin was enhanced. Splenic natural killer cell cytotoxicity was unchanged after suspension, which demonstrated the organ- and cell-specific effects of skeletal unloading. Whereas antiorthostatic suspension induced minimal changes in bone, there was a significant depression in the number of macrophage precursors in the bone marrow. Overall, skeletally unloaded animals had slightly higher blood corticosterone levels than did control animals; however, it did not appear to be responsible for the observed changes. In conclusion, skeletal unloading produces organ- and cell-specific changes in the murine immune system rather than a generalized immunosuppression.

摘要

使用抗重力尾部悬吊法使骨骼卸载对小鼠免疫系统的影响具有组织特异性。通过分析来自淋巴结、脾脏和骨髓的细胞证明了这一现象。抗重力悬吊11天后,淋巴结中植物血凝素诱导的T细胞增殖受到抑制。相比之下,脾脏中对植物血凝素产生反应的T细胞增殖增强。悬吊后脾脏自然杀伤细胞的细胞毒性没有变化,这证明了骨骼卸载对器官和细胞的特异性影响。虽然抗重力悬吊对骨骼的影响很小,但骨髓中巨噬细胞前体的数量却显著减少。总体而言,骨骼卸载的动物血液皮质酮水平略高于对照动物;然而,这似乎并不是观察到的变化的原因。总之,骨骼卸载在小鼠免疫系统中产生器官和细胞特异性变化,而非全身性免疫抑制。

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