@article { author = {Liu, Enna and Li, Zheng and Zhang, Yan and Chen, Kuisheng}, title = {Hepcidin Induces M1 Macrophage Polarization in Monocytes or THP-1 Derived Macrophages}, journal = {Iranian Journal of Immunology}, volume = {16}, number = {3}, pages = {190-199}, year = {2019}, publisher = {Shiraz Institute for Cancer Research}, issn = {1735-1383}, eissn = {1735-367X}, doi = {10.22034/iji.2019.80270}, abstract = {Background: Macrophage polarization plays a critical role in determining the inflammatory states. Hepcidin is a key negative regulator of iron homeostasis and functions. Although hepcidin has been shown to affect ferroportin expression in macrophages, whether it affects macrophage polarization is still largely unknown. Objective: To address whether hepcidin induces macrophage polarization. Methods: The expression of iNOS and CD206, and the ratio of IFN-γ vs IL-4 in THP-1 derived macrophages upon hepcidin stimulation were evaluated. Further detected was the percentage of CD16+ M1, CD23+ M1, CD10+ M2 and CCL22+ M2 cells in monocyte derived macrophages. Results: M1 associated molecules were increased in hepcidin-treated cells, yet M2 associated molecules were increased when hepcidin was neutralized. Concomitantly, we observed a significant increase in IRF3 phosphorylation in hepcidin-stimulated cells. However, STAT6 phosphorylation with hepcidin was neutralized. Conclusion: Hepcidin is able to induce macrophage polarization towards M1 type, and might be utilized as a potential M1 macrophage agonist in clinical practice.}, keywords = {Hepcidin,Macrophage,Polarization}, url = {https://iji.sums.ac.ir/article_45566.html}, eprint = {https://iji.sums.ac.ir/article_45566_e4dea11643d0b6a6fb4bbe2223235464.pdf} }