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Updated: Jul 31, 2025
12:08
Tracking Mouse Bone Marrow Monocytes In Vivo
Published on: February 27, 2015
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Energy saver: Monocytes hibernate in bone marrow upon fasting
Jan Tuckermann1, Pamela Fischer-Posovszky2
1Institute of Comparative Molecular Endocrinology, Ulm University, Ulm, Germany.
Cell Metabolism
|May 3, 2023
Summary
Fasting causes monocytes to move to bone marrow. Upon refeeding, these older immune cells worsen bacterial infections, highlighting nutrition
Area of Science:
- Immunology
- Nutritional Immunology
- Cellular Immunology
Background:
- Immune cell function is significantly modulated by nutritional status.
- Monocytes play a critical role in the innate and adaptive immune response.
- Understanding immune cell dynamics during nutritional changes is crucial for managing infections.
Purpose of the Study:
- To investigate the impact of fasting and refeeding on monocyte trafficking and function.
- To elucidate the role of glucocorticoids in mediating nutritional effects on monocytes.
- To determine the consequences of altered monocyte behavior on host defense during bacterial infection.
Main Methods:
- Utilized mouse models to study monocyte migration patterns.
- Assessed glucocorticoid levels during fasting and refeeding periods.
- Performed bacterial infection models to evaluate immune response and outcomes.
- Employed flow cytometry and cellular assays to characterize monocyte populations.
Main Results:
- Fasting induces glucocorticoid release, prompting monocytes to migrate from the bloodstream into the bone marrow.
- Refeeding leads to the release of these aged monocytes back into circulation.
- These older monocytes exhibit detrimental effects during bacterial infections, impairing host defense.
Conclusions:
- Nutritional status, specifically fasting and refeeding, dynamically regulates monocyte distribution and function.
- Glucocorticoid signaling is a key mediator of fasting-induced monocyte sequestration in the bone marrow.
- The chronological aging of monocytes during fasting impacts their immune function, potentially exacerbating infection severity.
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