RESEARCH ARTICLE
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
Article Information
Identifiers and Pagination:
Year: 2009Volume: 3
First Page: 81
Last Page: 85
Publisher ID: TODJ-3-81
DOI: 10.2174/1874372200903010081
Article History:
Received Date: 23/04/2009Revision Received Date: 11/05/2009
Acceptance Date: 04/06/2009
Electronic publication date: 28/7/2009
Collection year: 2009
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: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
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.
