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Aberrant wound healing in an epidermal interleukin-4 transgenic mouse model of atopic dermatitis

journal contribution
posted on 12.09.2016 by Y. Zhao, L. Bao, L. S. Chan, L. A. DiPietro, L. Chen
Wound healing in a pre-existing Th2-dominated skin milieu was assessed by using an epidermal specific interleukin-4 (IL-4) transgenic (Tg) mouse model, which develops a pruritic inflammatory skin condition resembling human atopic dermatitis. Our results demonstrated that IL-4 Tg mice had delayed wound closure and re-epithelialization even though these mice exhibited higher degrees of epithelial cell proliferation. Wounds in IL-4 Tg mice also showed a marked enhancement in expression of inflammatory cytokines/chemokines, elevated infiltration of inflammatory cells including neutrophils, macrophages, CD3+ lymphocytes, and epidermal dendritic T lymphocytes. In addition, these mice exhibited a significantly higher level of angiogenesis as compared to wild type mice. Furthermore, wounds in IL-4 Tg mice presented with larger amounts of granulation tissue, but had less expression and deposition of collagen. Taken together, an inflamed skin condition induced by IL-4 has a pronounced negative influence on the healing process. Understanding more about the pathogenesis of wound healing in a Th2- dominated environment may help investigators explore new potential therapeutic strategies.

Funding

This study was supported by NIH Grants R01GM50875 (LAD), College of Dentistry, University of Illinois at Chicago (LC, YZ, and LAD), Dr. Orville J. Stone Endowed Professorship (LSC), and the Albert H. and Mary Jane Slepyan Endowed Fellowship (LB).

History

Publisher Statement

This is a copy of an article published in the PLoS ONE. © 2016 Zhao et al.

Publisher

Public Library of Science

Language

en_US

issn

1932-6203

Issue date

11/01/2016

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