The skin's normal microflora – the microscopic and usually harmless bacteria that live on the skin – includes certain staphylococcal bacterial species that will induce an inflammatory response when they are introduced below the skin's surface, but do not initiate inflammation when present on the epidermis, or outer layer of skin.
In this study, Lai, Gallo and colleagues reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. Such inhibition is mediated by a molecule called staphylococcal lipoteichoic acid (LTA) which acts on keratinocytes – the primary cell types found on the epidermis.
The researchers also found that Toll-like receptor 3 (TLR3) activation is required for normal inflammation after skin injury.
"Keratinocytes require TLR3 to mount a normal inflammatory response to injury, and this response is kept from becoming too aggressive by staphylococcal LTA," said Gallo. "To our knowledge, these findings show for the first time that the skin epithelium requires TLR3 for normal inflammation after wounding and that the microflora helps to modulate this response."
Source-Eurekalert
ARU