Effects of platinum and palladium nanocolloid on macrophage polarization in relevance to repigmentation of vitiligo


Abstract

Background

Elevated oxidative stress is accepted to be the initial event in vitiligo leading to the final pathological regulation of immune systems known as autoimmune reaction, which destroys melanin‐forming cells, melanocytes. Recently, we reported an efficient topical use of PAPLAL, nanocolloid of platinum and palladium, having intense catalase‐like activity to vitiligo patients. In addition, we found that PAPLAL has dual effects on the AhR and Nrf‐2 pathways in keratinocytes, and suggested its contribution to the recovery of immune state in vitiligo. The precise mechanism developing autoimmune reaction in vitiligo, however, remains to be clarified. It is important to clarify what kinds of cells play an essential role in the development of vitiligo.

Objective

To further understand the effective mechanisms of PAPLAL on immunity of skin, and to confirm a role of autoimmunity in vitiligo development, we studied the effect of PAPLAL on macrophage polarization and its activities which are recognized to play a pivotal role in immune and inflammatory reactions in many organs.

Methods

Rat and human macrophages were cultured and stimulated in vitro with both LPS and IFN‐γ for M1 polarization and IL‐4 and IL‐13 for M2 polarization with or without PAPLAL. Expression of typical M1 and M2 markers was determined at mRNA and protein levels.

Results

Simultaneous treatment with PAPLAL suppressed remarkably the production of M1 markers, iNOS, and TNF‐α; further, PAPLAL also suppressed M2 markers, mannose receptor (Man R), Chitinase 3‐like 3 (YM‐1), and iron regulatory protein‐1 (IRP‐1), at mRNA and protein levels, but less effectively compared to those of M1. PAPLAL, however, did not suppress phagocytic activity of M0, M1, and M2 cells.

Conclusion

These results indicate that macrophages may be involved in the therapeutic potential of PAPAL by altering immunological environment disturbed in skin, with the delicate shift of the M1‐M2 polarization, but without affecting on phagocytic activity.

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