IL-5-overexpressing mice exhibit eosinophilia and altered wound healing through mechanisms involving prolonged inflammation

Victoria D. Leitch, Xanthe L. Strudwick, Klaus I. Matthaei, Lindsay A. Dent, Allison J. Cowin

    Research output: Contribution to journalArticlepeer-review

    40 Citations (Scopus)

    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.

    Original languageEnglish
    Pages (from-to)131-140
    Number of pages10
    JournalImmunology and Cell Biology
    Volume87
    Issue number2
    DOIs
    Publication statusPublished - Feb 2009

    Fingerprint

    Dive into the research topics of 'IL-5-overexpressing mice exhibit eosinophilia and altered wound healing through mechanisms involving prolonged inflammation'. Together they form a unique fingerprint.

    Cite this