Conflicts of interest None declared.
Impaired cutaneous wound healing in granulocyte/ macrophage colony-stimulating factor knockout mice
Article first published online: 6 JUN 2007
British Journal of Dermatology
Volume 157, Issue 3, pages 458–465, September 2007
How to Cite
Fang, Y., Gong, S.-J., Xu, Y.-H., Hambly, B.D. and Bao, S. (2007), Impaired cutaneous wound healing in granulocyte/ macrophage colony-stimulating factor knockout mice. British Journal of Dermatology, 157: 458–465. doi: 10.1111/j.1365-2133.2007.07979.x
- Issue published online: 10 AUG 2007
- Article first published online: 6 JUN 2007
- Accepted for publication 2 March 2007
- granulocyte/macrophage colony-stimulating factor;
- wound healing
Background Wound healing involves various cells and cytokines, resulting in the regular progression of remodelling events. Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a multifunctional pleiotropic cytokine and is known to facilitate wound healing, although the precise molecular and cellular mechanisms remain to be explored.
Objectives To use GM-CSF gene knockout (GM-CSF KO) mice to investigate the role of GM-CSF in cutaneous wound healing following full-thickness skin injury.
Methods Full-thickness skin wounds were made in GM-CSF KO and wild-type mice. The wound closure, leucocyte infiltration, vascularization and extent of cytokine production were determined.
Results Wound healing was significantly delayed in GM-CSF KO mice, accompanied by reduced cytokine production (interleukin-6, monocyte chemoattractant protein-1 and macrophage inflammatory protein-2), and platelet-endothelial cell adhesion molecule-1 expression. Consequently there was reduced recruitment of neutrophils and macrophages and reduced vascularization in the wounds of GM-CSF KO mice. Although collagen deposition was delayed, it was significantly increased in the wounds of the GM-CSF KO mice in the later stages of wound healing.
Conclusions We conclude that GM-CSF plays an important role in the complex network of effector molecules that regulate keratinocyte proliferation and the inflammatory response. These data have important implications for further development of the therapeutic manipulation of wound healing using GM-CSF.