Human β-Defensin-2 Expression by Keratinocytes is Induced by Co-Culture with Trycophyton rubrum Through Toll-Like Receptors 2 and 4

Hiroshi Ishikawa*, 1, SangJae Bae11, Ichiro Katayama1, 2
1 Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
2 Department of Dermatology, Osaka University Graduate School of Medicine, Osaka, Japan

© 2009 Ishikawa et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan; Tel: 81-95-819-7333; Fax: 81-95-819-7335; E-mail:


To determine a role of human β-Defensin-2 (HBD-2) in defense against cutaneous dermatophyte infection, we investigated the induction of HBD-2 mRNA expression by a nontumorigenic human keratinocyte-derived cell line, HaCaT cells, after co-culture with microconidia collected from the colonies of Trichophyton rubrum. Co-culture of T. rubrum or Candida albicans with HaCaT cells significantly induced HBD-2 mRNA expression. Furthermore, treatment with anti-TLR2 or TLR4 antibodies inhibited T. rubrum-induced HBD-2 upregulation, while it did not affect C. albicans-induced HBD-2 upregulation. Pretreatment of T. rubrum with Concanavalin A, which blocks mannosyl and glucosyl residues, inhibited HBD-2 expression by HaCaT cells, suggesting that mannosylated and glycosylated residues are important for HBD-2 induction. Collectively, these results suggest that T. rubrum induces HBD-2 expression through TLR2 and/or TLR4 pathway in keratinocytes and that HBD-2 may play a defense role in cutaneous dermatophyte infection.

Keywords: Human-defensin-2, Trichophyton rubrum, Candida albicans, keratinocyte, toll-like receptor.