1163 Skin commensal bacteria modulate ultraviolet radiation-induced cytokine secretion in human keratinocytes

Exposure of skin to ultraviolet radiation (UVR) induces immunosuppression and is associated with induction of interleukin (IL)-10. In mice, the presence of a cutaneous microbiome elevates the expression of pro-inflammatory mediators (IL-6, chemokine; CCL20), which is thought to reduce UVR-induced immunosuppression. However, there is little understanding of how or which human skin commensals may contribute to the regulation of UVR-induced immunosuppression. Here, we present evidence of skin commensal-dependent regulation of UVR-induced immunosuppressive (IL-10) and pro-inflammatory (IL-6/CCL20) mediators. Normal human epidermal keratinocytes (NHEKs) received a single dose (erythemally-weighted, 20mJ/cmˆ2) of narrowband UVB in the presence or absence of Micrococcus luteus (1x10ˆ4 CFU/ml), Staphylococcus hominis (1x10ˆ2 CFU/ml) or Cutibacterium acnes (1x10ˆ6 CFU/ml). NHEK viability and secretion of IL-10, IL-6, and CCL20 were assessed 24 h post-irradiation. UVR exposure resulted in a mean 37% decrease in NHEK viability compared to control unirradiated cells (p<0.05). M. luteus partially abrogated UVR induced cytotoxicity resulting in a 19% increase in cell viability relative to the 20mJ/cmˆ2 irradiated control (p<0.05), which was accompanied by 35% and 39% decreases in IL-10 (p<0.05) and CCL20 (p<0.05) secretion respectively relative to the irradiated control. C. acnes and S. hominis had no significant effect on NHEK viability, but C. acnes reduced IL-10 secretion by 20% (p<0.0001) and increased IL-6 secretion by 67% (p<0.05) relative to the respective irradiated controls. In conclusion, specific skin commensal bacteria are capable of differentially regulating UVR-induced responses in keratinocytes. These data suggest a role for the human microbiome in the response of human skin to UVR.