GM-CSF promotes pro-inflammatory macrophage activation associated with Akt/mTOR signaling during experimental colitis
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By
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Silan Shen
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Kexin Chen
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Lili Li
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Mingshan Jiang
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Yongbin Jia
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Xiufeng Bai
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Zhen Zeng
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Chunxiang Ma
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Yuan Dang
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Kehan Hu
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Yanqiong Chen
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Wenting Zhang
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Zhiyong Miao
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Linlin Chen
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Hu Zhang
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June 26, 2026
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Clinical Scorecard: GM-CSF Enhances Pro-Inflammatory Macrophage Activation Linked to Akt/mTOR Pathway in Experimental Colitis
At a Glance
| Category | Detail |
|---|
| Condition | Ulcerative Colitis |
| Key Mechanisms | GM-CSF modulates macrophage function and promotes inflammation via the Akt/mTOR pathway. |
| Target Population | Patients with Ulcerative Colitis |
| Care Setting | Clinical research and experimental models |
Key Highlights
- GM-CSF expression is elevated in colon tissues of UC patients.
- GM-CSF neutralizing antibody reduces gut inflammation in DSS-induced colitis mice.
- GM-CSF induces M1-type polarization of macrophages and enhances Th17 responses.
- The proinflammatory effects of GM-CSF are linked to glycolytic metabolism.
- The Akt/mTOR pathway is involved in GM-CSF's modulation of macrophage function.
Guideline-Based Recommendations
Diagnosis
- Assess GM-CSF levels in colon biopsy tissues for potential correlation with UC.
Management
- Consider GM-CSF neutralizing antibodies as a therapeutic strategy in UC.
Monitoring & Follow-up
- Monitor macrophage infiltration and polarization in UC patients.
Risks
- Overactivation of proinflammatory macrophages may exacerbate UC symptoms.
Patient & Prescribing Data
Patients diagnosed with Ulcerative Colitis.
Targeting GM-CSF may provide a new avenue for managing UC-related inflammation.
Clinical Best Practices
- Evaluate the role of macrophage polarization in UC pathogenesis.
- Investigate metabolic pathways influencing macrophage function in UC.
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