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Staphylococcus aureus  is one of the clinically most relevant pathogens causing infections. Humans are often exposed to  S. aureus . In approximately one-third of the healthy population it can be found on the skin either for long or short periods as colonizing “commensals”, without inducing infections or an inflammatory immune response. While tolerating  S. aureus  seems to be limited to certain individuals and time periods in most cases,  Staphylococcus epidermidis  is tolerated permanently on the skin of almost all individuals without activating overwhelming skin inflammation. To investigate this, we co-cultured a keratinocyte cell line (HaCaT) with viable  S. aureus  or  S. epidermidis  to study the differences in the immune activation . S. aureus  activated keratinocytes depicted by a profound IL-6 and IL-8 response, whereas  S. epidermidis  did not. Our data indicate that internalization of  S. aureus  and the subsequent intracellular sensing of bacterial nucleic acid may be essential for initiating inflammatory response in keratinocytes. Internalized dsRNA activates IL-6 and IL-8 release, but not TNF-α or IFNs by human keratinocytes. This is a non-specific effect of dsRNA, which can be induced using Poly(I:C), as well as RNA from  S. aureus  and  S. epidermidis . However, only viable  S. aureus  were able to induce this response as these bacteria and not  S. epidermidis  were actively internalized by HaCaT. The stimulatory effect of  S. aureus  seems to be independent of the TLR3, -7 and -8 pathways.

Inflammatory Response Against Staphylococcus aureus via Intracellular Sensing of Nucleic Acids in Keratinocytes