GM-CSF promotes pro-inflammatory macrophage activation associated with Akt/mTOR signaling during experimental colitis

To investigate the role of GM-CSF in ulcerative colitis (UC) and its mechanism of action on macrophage activation.

GM-CSF Expression Analysis: Examined GM-CSF expression in colon biopsy tissues from UC patients and healthy controls.
Animal Model Study: Utilized a DSS-induced colitis mouse model to evaluate the effects of GM-CSF neutralizing antibody.
In Vitro Experiments: Assessed macrophage polarization and glycolysis-related genes in response to GM-CSF.
Pathway Analysis: Investigated the involvement of the Akt/mTOR signaling pathway in macrophage activation.

GM-CSF expression was significantly elevated in colon biopsy tissues from UC patients compared to healthy controls.
Administration of GM-CSF neutralizing antibody (GM-CSF Ab) to DSS-treated mice reduced gut inflammation.
GM-CSF Ab inhibited macrophage and inflammatory CD4+ Th cell infiltration in DSS-colitis mice.
GM-CSF induced M1-type polarization of macrophages and enhanced Th17 responses.
The proinflammatory macrophage phenotype induced by GM-CSF was linked to glycolytic metabolism via the Akt/mTOR pathway.

GM-CSF is associated with macrophage activation and intestinal inflammation through modulation of glycolytic metabolism and the Akt/mTOR pathway.

The study primarily focused on animal models and human biopsy samples, which may not fully represent all aspects of UC pathology.
Further research is needed to clarify the dual role of GM-CSF in different inflammatory contexts.

GM-CSF plays a significant role in promoting intestinal inflammation by regulating macrophage function and metabolism.