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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: fj.07-104117v1 22/7/2168    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Abtin, A. Articles by Tschachler, E. Search for Related Content PubMed PubMed Citation Articles by Abtin, A. Articles by Tschachler, E.

Flagellin is the principal inducer of the antimicrobial peptide S100A7c (psoriasin) in human epidermal keratinocytes exposed to Escherichia coli

Arby Abtin^*, Leopold Eckhart^*, Michael Mildner^*, Florian Gruber^*, Jens-Michael Schröder and Erwin Tschachler^*,,1

^* Department of Dermatology, Medical University of Vienna, Vienna, Austria;

Department of Dermatology, University Hospital Schleswig-Holstein, University of Kiel, Kiel, Germany; and

Centre de Recherches et d'Investigations Epidermiques et Sensorielles, Neuilly sur Seine, France

¹Correspondence: Department of Dermatology, Medical University of Vienna, Waehringer Guertal 18–20, 1090 Vienna, Austria. E-mail: erwin.tschachler{at}meduniwien.ac.at

Epidermal keratinocytes (KCs) express antimicrobial peptides as a part of the innate immune response. It has recently been shown that the culture supernatant of Escherichia coli induces the expression of S100A7c (psoriasin) in KCs and that S100A7c efficiently kills E. coli. Here we have investigated which of the microbial components triggers the up-regulation of S100A7c expression. Exposure of human primary KCs to ligands of the human Toll-like receptors (TLRs) revealed that only the TLR5 ligand flagellin strongly induced the expression of S100A7c mRNA and protein, whereas all other TLR ligands had no significant effect. In contrast to the supernatant from flagellated wild-type (WT) E. coli, the supernatant of a flagellin-deficient E. coli strain (FliC) did not induce S100A7c expression. Small interfering RNA-mediated knockdown of TLR5 expression suppressed the ability of KCs to up-regulate S100A7c expression in response to both flagellin and WT E. coli supernatant. Taken together, our data demonstrate that bacterial flagellin is essential and sufficient for the induction of S100A7c expression in KCs by E. coli.—Abtin, A., Eckhart, L., Mildner, M., Gruber, F., Schröder, J.-M., Tschachler, E. Flagellin is the principal inducer of the antimicrobial peptide S100A7c (psoriasin) in human epidermal keratinocytes exposed to Escherichia coli.

Key Words: innate immunity • Toll-like receptor • TLR • pathogen-associated molecular pattern • PAMP • antimicrobial defense