Commensal bacteria regulate Toll-like receptor 3-dependent inflammation after skin injury

Lai, Y; di Nardo, A; Nakatsuji, T; Leichtle, A; Yang, Y; Cogen, AL; Wu, ZR; Hooper, LV; Schmidt, RR; von Aulock, S; Radek, KA; Huang, CM; Ryan, AF; Gallo, RL; (2009) Commensal bacteria regulate Toll-like receptor 3-dependent inflammation after skin injury. Nature medicine, 15 (12). pp. 1377-82. ISSN 1078-8956 DOI:

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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. Here we reveal 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 triggered through Toll-like receptor 3(TLR3). We show that TLR3 activation is required for normal inflammation after injury and that keratinocytes require TLR3 to respond to RNA from damaged cells with the release of inflammatory cytokines. 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.

Item Type: Article
Keywords: Humans, Inflammation/*microbiology, Skin Diseases, Bacterial/*physiopathology, Staphylococcal Infections/*physiopathology, Toll-Like Receptor 3/*physiology, Humans, Inflammation, microbiology, Skin Diseases, Bacterial, physiopathology, Staphylococcal Infections, physiopathology, Toll-Like Receptor 3, physiology
Faculty and Department: Faculty of Infectious and Tropical Diseases > Dept of Clinical Research
PubMed ID: 19966777
Web of Science ID: 272407800017


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