Critical role of the GM-CSF signaling pathway in macrophage pro-repair activities
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Updated: Apr 25, 2026

Neuron-Macrophage Co-cultures to Activate Macrophages Secreting Molecular Factors with Neurite Outgrowth Activity
Published on: March 30, 2018
Eric Bernasconi1, Fabrizia D'Angelo, Pierre Michetti
1Service of Gastroenterology and Hepatology, Department of Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland.
Objective:
Macrophages play a critical role in intestinal wound repair. However, the molecular pathways that regulate macrophage wound repair activities remain poorly understood. The aim of this study was to evaluate the role of GM-CSF receptor signaling in the wound repair activities of macrophages.
Methods:
Murine macrophages were differentiated from bone marrow cells and human macrophages from monocytes isolated from peripheral blood mononuclear cells of Crohn's disease (CD) patients. In vitro models were used to study the repair activities of macrophages.
Results:
We provide evidence that GM-CSF receptor signaling is required for murine macrophages to promote epithelial repair. In addition, we demonstrate that the deficient repair properties of macrophages from CD patients with active disease can be recovered via GM-CSF therapy.
Conclusion:
Our data support a critical role of the GM-CSF signaling pathway in the pro-repair activities of mouse and human macrophages.
Insights
Granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor signaling is essential for macrophage-driven intestinal wound repair. GM-CSF therapy can restore repair functions in macrophages from Crohn
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Macrophages are crucial for intestinal wound healing.
- Molecular mechanisms regulating macrophage pro-repair functions are not fully understood.
Purpose of the Study:
- To investigate the role of Granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor signaling in macrophage-mediated intestinal wound repair.
- To evaluate GM-CSF therapy for restoring repair functions in macrophages from Crohn's disease patients.
Main Methods:
- Differentiated murine bone marrow cells into macrophages.
- Isolated human monocytes from Crohn's disease patients for macrophage differentiation.
- Utilized in vitro models to assess macrophage repair activities.
Main Results:
- GM-CSF receptor signaling is necessary for murine macrophages to promote epithelial repair.
- Macrophages from Crohn's disease patients with active disease exhibited deficient repair properties.
- GM-CSF therapy successfully restored the repair capabilities of these macrophages.
Conclusions:
- The GM-CSF signaling pathway plays a vital role in the pro-repair functions of both mouse and human macrophages.
- GM-CSF represents a potential therapeutic target for enhancing intestinal wound repair in conditions like Crohn's disease.
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