Commensal bacteria regulate Toll-like receptor 3-dependent inflammation after skin injury (Nat Med, 2009, 15:1377-1382)

報告日期: 2010/05/25
報告時間: 16:00/16:50
報告學生: 李易丞
講評老師: 楊倍昌

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


Yuping Lai1,2, Anna Di Nardo1,2, Teruaki Nakatsuji1,2, Anke Leichtle2,3, Yan Yang4, Anna L Cogen1,2, Zi-Rong Wu4,Lora V Hooper5, Richard R Schmidt6, Sonja von Aulock6, Katherine A Radek1,2, Chun-Ming Huang1,2,Allen F Ryan2,3 & Richard L Gallo1,2,7

Nat Med. 2009 Dec;15(12):1377-82. Epub 2009 Nov 22




Date25 May, 2010  16:10~17:00

PlaceRoom 602



There are many complex metazoans colonized on the inter- or outer- surface of the body. Some of these microbial organisms are called ‘commensal microflora’ is a group of microorganism that are huntless even beneficial for human health. Probiotics is a group of microbiome, as well known, they can regulate cytokine expression profile to suppress intestine inflammation condition of the host. Staphylococcal species are commensal bacteria of the skin, and they can induce inflammation when present below the dermis, but tolerated with epidermal surface. By this way, authors suggest that these microbes may have some regulating mechanism to inhibit the inflammation response, and it may be the regulating mechanism of wound healing inflammation. In this study, they found that staphylococcus’ lipoteichoic acid (LTA) is the functional compound to block the over inflammation response. Skin injury inflammation signal was transduced by Toll-like receptor 2 (TLR2) through NF-κB to prime TNF-α and IL-6 and it’s blocked by staphylococcus’ LTA through TLR3 pathway.



1.     Steidler, L. et al. Treatment of murine colitis by Lactococcus lactis secreting interleukin-10. Science 289, 1352–1355 (2000).

2.     Vandenbroucke, K. et al. Active delivery of trefoil factors by genetically modified Lactococcus lactis prevents and heals acute colitis in mice. Gastroenterology 127, 502–513 (2004).

3.     Haller, D. et al. Transforming growth factor-β1 inhibits nonpathogenic Gram negative bacteria–induced NF-κB recruitment to the interleukin-6 gene promoter in intestinal epithelial  cells through modulation of histone acetylation. J. Biol. Chem. 278, 23851–23860 (2003).