1. ¹Women's and Children's Health Research Institute, North Adelaide, South Australia
2. ²Division of Molecular Bioscience, The John Curtin School of Medical Research, Canberra, ACT, Australia
3. ³School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia
4. ⁴Discipline of Surgery, University of Adelaide, Adelaide, South Australia

Correspondence: Dr AJ Cowin, Women's and Children's Health Research Institute, 72 King William Road, North Adelaide 5066, South Australia. E-mail: allison.cowin@adelaide.edu.au

Received 26 May 2008; Revised 28 August 2008; Accepted 1 September 2008; Published online 7 October 2008.

Abstract

Leucocytes are essential in healing wounds and are predominantly involved in the inflammatory and granulation stages of wound repair. Eosinophils are granulocytic leucocytes and are specifically regulated by interleukin-5 (IL-5), a cytokine produced by T helper 2 (Th2) cells. To characterize more clearly the role of the IL-5 and eosinophils in the wound healing process, IL-5-overexpressing and IL-5-deficient mice were used as models of eosinophilia and eosinophil depletion, respectively. Our results reveal a significantly altered inflammatory response between IL-5-overexpressing and IL-5 knockout mice post-wounding. Healing was significantly delayed in IL-5-overexpressing mice with wounds gaping wider and exhibiting impaired re-epithelialization. A delay in collagen deposition was observed suggesting a direct effect on matrix synthesis. A significant increase in inflammatory cell infiltration, particularly eosinophils and CD4⁺ cells, one of the main cell types which secrete IL-5, was observed in IL-5-overexpressing mice wounds suggesting that one of the main roles of IL-5 in wound repair may be to promote the infiltration of eosinophils into healing wounds. Healing is delayed in IL-5-overexpressing mice and this corresponds to significantly increased levels of eosinophils and CD4⁺ cells within the wound site that may contribute to and exacerbate the inflammatory response, resulting in detrimental wound repair.