Electrogenic Staphylococcus epidermidis Diminishes the Ultraviolet B-Induced Labile Irons in Mouse Skin

The tremendous abundance of Staphylococcus epidermidis (S. epidermidis) on the skin surface have been found electrogenic. However, the role of electrogenic S. epidermidis in biological activities remains elusive. Addition of S. epidermidis plus glycerol reinstated the reduction of electric currents of vancomycin-treated human skin bacteria collected by skin swabs. In the presence of glycerol, an endogenous molecule in human skin, S. epidermidis exerted the electrogenicity measured by the changes in voltages and currents as well as ferrozine assays. A substantial increase in iron contents in skin was detected when mouse skin was exposed to ultraviolet B (UV-B). Topical application of S. epidermidis plus glycerol onto mouse skin mitigated the UV-B-induced production of labile ferrous iron, demonstrating that S. epidermidis electricity acted as a regulator of the redox cycling of irons in skin. Low expression of cyclophilin A, an electron mediator, in S. epidermidis caused the loss of bacterial activities to reduce the UV-B-induced labile ferrous iron. Cumulatively, skin electrogenic S. epidermidis may mediate cyclophilin A to combat the UV-B-induced iron imbalance in skin.