Commensal bacteria regulate Toll-like receptor 3–dependent inflammation after skin injury.
The normal microflora of the skin includes staphylococcal species that will induce inflammation when present below the dermis but are tolerated on the epidermal surface without initiating inflammation. This research indicates a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. This inhibition is mediated by staphylococcal lipoteichoic acid (LTA) and acts selectively on keratinocytes. Activation is required for normal inflammation after injury. Staphylococcal LTA inhibits both inflammatory cytokine release from keratinocytes and inflammation triggered by injury through a TLR2-dependent mechanism. 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 can modulate specific cutaneous inflammatory responses. Nat Med. 2009 Dec;15(12):1377-82. Epub 2009 Nov 22.
Publication Type: Journal article
Publisher: Nature Medicine