Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/53417
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Type: Journal article
Title: IL-5-overexpressing mice exhibit eosinophilia and altered wound healing through mechanisms involving prolonged inflammation
Author: Leitch, V.
Strudwick, X.
Matthaei, K.
Dent, L.
Cowin, A.
Citation: Immunology and Cell Biology, 2009; 87(2):131-140
Publisher: Blackwell Publishing Asia
Issue Date: 2009
ISSN: 0818-9641
1440-1711
Statement of
Responsibility: 
Victoria D Leitch. Xanthe L Strudwick, Klaus I Matthaei, Lindsay A Dent and Allison J Cowin.
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.
Keywords: wound; eosinophil; IL-5
RMID: 0020083753
DOI: 10.1038/icb.2008.72
Appears in Collections:Molecular and Biomedical Science publications

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