Objective:

Tinospora cordifolia is a plant with several medicinal properties. However, the effect of T. cordifolia extract on macrophage polarization is not known. Here we report a detailed analysis of the impact of T. cordifolia extract on the polarization of primary human monocyte-derived macrophages.

Materials and Methods:

Macrophages, derived from human peripheral blood mononuclear cells monocytes (M0 macrophages), were either left untreated or pretreated with T. cordifolia extract at doses of 50 μg/mL, 100 μg/mL, 500 μg/mL, or 1.000 μg/mL for 2 h. Macrophages were then polarized into M1 (LPS, IFNγ), M2a (IL-4), or M2c (IL-10) macrophages for 22 h. M1 (HLA-DR, CD64, CD86) and M2 (CD200R, CD206, CD163) surface markers were analyzed by flow cytometry. The M1 cytokine tumor necrosis factor (TNF) was analyzed by Enzyme-linked Immunosorbent Assay.

Results:

Our data demonstrated that in M0 macrophages, T. cordifolia extract treatment increased the expression of the M1 marker CD86 (p=0.0036), while it decreased the expression of the M2a marker CD200R (p=0.0059). In M2a and M2c macrophages, T. cordifolia extract decreased the expression of the M2a marker CD200R (p=0.0098) and the M2c marker CD163 (p=0.0173), respectively. Interestingly, after treatment with T. cordifolia extract, the phagocytic receptors CD64 (p<0.0001) and CD206 (p<0.0001) were upregulated in M0, M1, M2a, and M2c macrophages. Finally, T. cordifolia extract treatment enhanced the production of TNF in M0, M2a, and M2c macrophages.

Conclusion:

Overall, our data suggest that T. cordifolia extract shifts the polarization of primary human macrophages into a pro-inflammatory M1 phenotype, with an upregulation of the phagocytic receptors CD64 and CD206.

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