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The effects of rM-CSF and rIL-6 therapy on immunosuppressed antiorthostatically suspended mice
J W Armstrong1, K Kirby-Dobbels, S K Chapes
1Division of Biology, Kansas State University, Manhattan 66506, USA.
Abstract:
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.
Insights
Antiorthostatic suspension suppressed macrophage development by reducing macrophage colony-stimulating factor (M-CSF). Recombinant M-CSF therapy restored macrophage development, indicating M-CSF
Area of Science:
- Space biology and immunology
- Bone biology and immunology
Background:
- Antiorthostatic suspension, a model for microgravity, suppresses macrophage development in bone.
- Bone marrow cells in suspended mice show reduced secretion of macrophage colony-stimulating factor (M-CSF) and interleukin-6 (IL-6).
- M-CSF and IL-6 are critical for bone marrow macrophage maturation.
Purpose of the Study:
- To investigate the role of M-CSF and IL-6 in suppressed macrophage development during antiorthostatic suspension.
- To determine if M-CSF or IL-6 therapy can reverse the effects of antiorthostatic suspension on macrophage development.
Main Methods:
- Mice were subjected to antiorthostatic suspension.
- Bone marrow cells were analyzed for M-CSF and IL-6 secretion.
- Recombinant M-CSF or IL-6 was administered intraperitoneally to treated mice.
- Macrophage development was assessed in treated and control mice.
Main Results:
- Antiorthostatic suspension suppressed macrophage development in both loaded and unloaded bones.
- Bone marrow cells from suspended mice secreted significantly less M-CSF and IL-6 compared to controls.
- Recombinant M-CSF therapy successfully reversed the suppressive effects of suspension on macrophage development.
- Recombinant IL-6 therapy did not reverse the suppressive effects.
Conclusions:
- Depressed levels of M-CSF, not IL-6, contribute to inhibited bone marrow macrophage progenitor maturation under antiorthostatic suspension.
- Bone marrow cells producing M-CSF are sensitive to the effects of antiorthostatic suspension.
- M-CSF is a key factor in maintaining macrophage development during simulated microgravity.