TGFβ-1 Modulates M1/M2 Macrophage Axis: Implications for Tissue Regeneration

Objectives: Shed light on the mechanism of TGFβ-1 in inflammation and odontogenesis, and the possibility of TGFβ-1 being used for targeted pulp regeneration.
Methods: THP-1 cells that were maintained in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) were differentiated to the nonpolarized M0 macrophage type by exposure to 100 nmol/L phorbol 12-myristate 13-acetate (PMA) for 2 days. The M0 macrophages were polarized to the M1 and M2 phenotypes by treatment with IFN-γ/LPS and IL-4, respectively, for two days with the addition of TGFβ-1 added at the concentration of 50ng/mL, 10ng/mL, 1ng/mL, or 0 ng/mL. The cells were then collected for RNA extraction, reverse transcription, and then amplification. M1 and M2 phenotype markers were evaluated by RT-PCR.
Results: No statistically significant difference was seen in the expression of pro-inflammatory M1 and anti-inflammatory M2 with the addition of TGFβ-1 in both M0 and M1.
Conclusions: The present findings suggest that TGFβ-1 mediates M1/M2 axis of macrophages. Our work continues to further probe molecular mechanisms of TGFβ-1 signaling on the complex roles of macrophages on inflammation. Our next approach would be to change the parameters to first make sure TGFβ-1 polarizes M0 to M1. Then we can test its effect on M1 polarization into M2.