Research data supporting: Skin Staphylococcus species Differentially Modulate Keratinocyte Cytokine Secretion in Response to UVB

Skin acts as the body’s first line of defence against environmental insults including ultraviolet radiation (UVR) from sunlight and participates in a dialog with its resident skin microbiota, increasingly recognised for its role in shaping and educating the immune responses of the skin in both health and disease. However, how or indeed if it mediates inflammatory responses to sunlight remains unclear. To address this, we investigated the effects of five abundant members of the skin microbiota on cytokine secretion in human primary keratinocytes exposed to a single dose of UVB. Co-culture of primary keratinocytes with a defined 5-species skin commensal community resulted in a non-selective increase in the secretion of innate immune mediators including interleukin-6 (IL-6), independent of UVB exposure. In the absence of UVB, Staphylococcus epidermidis was the dominant species, followed by Staphylococcus hominis within the 5-species community. UVB induced a marked shift in community composition, characterised by increased proliferation of Staphylococcus hominis and reduced Staphylococcus epidermidis abundance, as confirmed by species-specific growth curve analyses. Assessment of species-specific effects using mono-associated host cells revealed S. epidermidis as the predominant contributor to the enhancement of immune mediator secretion. Without the presence of additional community members, UVB amplified S. epidermidis induced cytokine secretion. However, co-culture of S. epidermidis with S. hominis attenuated the heightened inflammatory response to UVB typically associated with S. epidermidis, likely due to the reduced abundance of S. epidermidis following UVB exposure. These findings suggest that our resident skin microbiota may contribute to our inflammatory response to sunlight.