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Potent and Broad-Spectrum Antimicrobial Activity of CXCL14 Suggests an Immediate Role in Skin Infections¹

Christa Maerki^*, Simone Meuter, Mark Liebi^*, Kathrin Mühlemann, Mitchell J. Frederick^¶, Nikhil Yawalkar, Bernhard Moser^2, and Marlene Wolf^2,3,*

^* Theodor Kocher Institute, Institute for Infectious Diseases, and Department of Dermatology, University of Bern, Bern, Switzerland; Department of Medical Biochemistry and Immunology, Cardiff University School of Medicine, Cardiff, United Kingdom; and ^¶ Department of Head and Neck Surgery, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030

The skin is constantly exposed to commensal microflora and pathogenic microbes. The stratum corneum of the outermost skin layer employs distinct tools such as harsh growth conditions and numerous antimicrobial peptides (AMPs) to discriminate between beneficial cutaneous microflora and harmful bacteria. How the skin deals with microbes that have gained access to the live part of the skin as a result of microinjuries is ill defined. In this study, we report that the chemokine CXCL14 is a broad-spectrum AMP with killing activity for cutaneous Gram-positive bacteria and Candida albicans as well as the Gram-negative enterobacterium Escherichia coli. Based on two separate bacteria-killing assays, CXCL14 compares favorably with other tested AMPs, including human β-defensin and the chemokine CCL20. Increased salt concentrations and skin-typical pH conditions did not abrogate its AMP function. This novel AMP is highly abundant in the epidermis and dermis of healthy human skin but is down-modulated under conditions of inflammation and disease. We propose that CXCL14 fights bacteria at the earliest stage of infection, well before the establishment of inflammation, and thus fulfills a unique role in antimicrobial immunity.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Staatssekretariat für Bildung und Forschung Grant 03.04412 and European Framework Programme No. 6 Grant 518167.

² B.M. and M.W. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Marlene Wolf, Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012 Bern, Switzerland. E-mail address: marlene.wolf{at}tki.unibe.ch

⁴ Abbreviations used in this paper: DC, dendritic cell; AMP, antimicrobial peptide; HBD, human β-defensin; MEC, minimal effective concentration; RDU, radial diffusion unit; S. coag.neg. spp., coagulase-negative Staphylococcus spp.