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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Movement / drug effects
  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Humans
  • Keratinocytes / cytology
  • Keratinocytes / drug effects*
  • Keratinocytes / immunology
  • Lectins, C-Type / metabolism*
  • Polysaccharides, Bacterial / immunology
  • Polysaccharides, Bacterial / pharmacology*
  • Re-Epithelialization / drug effects*
  • Re-Epithelialization / immunology
  • Skin
  • beta-Glucans / immunology
  • beta-Glucans / pharmacology*

Substances

  • CLEC7A protein, human
  • Lectins, C-Type
  • Polysaccharides, Bacterial
  • beta-Glucans
  • curdlan