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Cell Immunol. 2014 May-Jun;289(1-2):49-54. doi: 10.1016/j.cellimm.2014.03.007. Epub 2014 Mar 27.

Dectin-1 activation induces proliferation and migration of human keratinocytes enhancing wound re-epithelialization.

Author information

1
Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
2
Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands; Euro Skin Bank, Beverwijk, The Netherlands.
3
Department of Plastic, Reconstructive and Hand Surgery, VU University Medical Center, Amsterdam, The Netherlands; Association of Dutch Burn Centres, Beverwijk, The Netherlands.
4
Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Electronic address: t.b.geijtenbeek@amc.uva.nl.

Abstract

Beta-glucans in temporary wound dressings have immuno-stimulatory capacities and have been shown to enhance wound healing in burn patients. Curdlan is a 1,3-linked bacterial/fungal derived beta-glucan that induces inflammatory responses via the C-type lectin receptor dectin-1 on dendritic cells (DCs). Here we investigated the effect of beta-glucan curdlan and the role of dectin-1 expressed by keratinocytes (KCs) in wound healing. Curdlan enhanced migration, proliferation and wound closure of human KCs in a dectin-1 dependent manner, both in vitro and ex vivo. Our data suggest that curdlan induces human KC proliferation and migration and could therefore be used in creams to enhance wound healing.

KEYWORDS:

Beta-glucans; Dectin-1; Keratinocytes; Migration; Proliferation; Wound healing

PMID:
24721111
DOI:
10.1016/j.cellimm.2014.03.007
[Indexed for MEDLINE]

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