Abstract
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.
Highlights
Wound healing is a well-regulated complicated process that involves interactions among resident and recruited cells such as epithelial cells, fibroblasts, endothelial cells, inflammatory cells, and interactions of those cells with extracellular matrix molecules, growth factors, cytokines, and chemokines
Wound closure in IL-4 Tg mice was delayed compared to wild type (WT) mice; this delay was statistically significant at days 5, 7, and 10 (Fig 1A and 1B)
The results clearly showed that skin wound healing in IL-4 Tg mice was severely impaired, the wounds eventually healed without signs of infections or excessive scar formation
Summary
Wound healing is a well-regulated complicated process that involves interactions among resident and recruited cells such as epithelial cells, fibroblasts, endothelial cells, inflammatory cells, and interactions of those cells with extracellular matrix molecules, growth factors, cytokines, and chemokines. Inflammatory response is a normal part of the healing process following injury that helps eliminate micro-organisms and injured cells. Excessive inflammation may be unfavorable to subsequent healing [1,2,3]. IL-4 is mainly secreted by Th2 cells, mast cells, eosinophils, and basophils. It was first identified as a factor promoting the growth and differentiation of B lymphocytes [4].
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