S100A15, an antimicrobial protein of the skin:: Regulation by E-coli through toll-like receptor 4

被引:61
作者
Buechau, Amanda S. [1 ]
Hassan, Mohamed
Kukova, Gabriela
Lewerenz, Virginia
Kellermann, Sabine
Wuerthner, Jens U.
Wolf, Ronald
Walz, Markus
Gallo, Richard L.
Ruzicka, Thomas
机构
[1] Univ Calif San Diego, Div Dermatol, San Diego, CA 92307 USA
[2] Univ Dusseldorf, Dept Dermatol, D-4000 Dusseldorf, Germany
[3] VA San Diego Healthcare Syst, San Diego, CA USA
[4] Univ Dusseldorf, Dept Med Microbiol, D-4000 Dusseldorf, Germany
[5] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA
[6] Univ Munich, Dept Dermatol, D-8000 Munich, Germany
关键词
D O I
10.1038/sj.jid.5700946
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
E. coli is a Gram-negative bacterium rarely found on human skin. We investigated whether direct interaction of E. coli with keratinocytes might induce an innate immune response through recognition by pattern recognition receptors. The capacity of E. coli to activate innate immune responses and IL-8 induction was investigated. We found that E. coli significantly induced human S100A7 and S100A15 transcript abundance and IL-8 release in cultured primary human keratinocytes. S100A15 is a member of the S100 protein family with previously unknown function. E. coli induced effects could be inhibited by neutralizing Toll-like receptor 4 (TLR4) antibodies, suggesting that E. coli-induced IL-8 and S100A15 expression in human keratinocytes are TLR4 dependent. TLR4(-/-) mice lacked elevated mS100A15 expression after infection with E. coli in contrast to wildtype mice. In vitro, human S100A15 displayed antimicrobial activity against E. coli. Our findings suggest that E. coli modulates S100A15 and IL-8 expression of keratinocytes by recognition through TLR4.
引用
收藏
页码:2596 / 2604
页数:9
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