Staphylococcus epidermidis WF2R11 Suppresses PM(2.5)-Mediated Activation of the Aryl Hydrocarbon Receptor in HaCaT Keratinocytes

The skin supports a diverse microbiome whose imbalance is related to skin inflammation and diseases. Exposure to fine particulate matter (PM(2.5)), a major air pollutant, can adversely affect the skin microbiota equilibrium. In this study, the effect and mechanism of PM(2.5) exposure in HaCaT keratinocytes were investigated. PM(2.5) stimulated the aryl hydrocarbon receptor (AhR) to produce reactive oxygen species (ROS) in HaCaT cells, leading to mitochondrial dysfunction and intrinsic mitochondrial apoptosis. We observed that the culture medium derived from a particular skin microbe, Staphylococcus epidermidis WF2R11, remarkably reduced oxidative stress in HaCaT cells caused by PM(2.5)-mediated activation of the AhR pathway. Staphylococcus epidermidis WF2R11 also exhibited inhibition of ROS-induced inflammatory cytokine secretion. Herein, we demonstrated that S. epidermidis WF2R11 could act as a suppressor of AhRs, affect cell proliferation, and inhibit apoptosis. Our results highlight the importance of the clinical application of skin microbiome interventions in the treatment of inflammatory skin diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12602-022-09922-8.