DescriptionA classical skin wound healing model can be divided into four distinct phases – instantaneous response, inflammatory, proliferation and the final remodeling phase. The balance between stimulatory and inhibitory mediators in each of these phases is critical in achieving optimal and efficient wound closure. It is well understood that inefficient or untimely resolution of inflammatory responses can result in profound delay in wound closure and increased tissue scarring as in the case with chronic wounds. This thesis studies the impact of exogenous administration of different types of pro inflammation resolution compounds such as Resolvin E1 (RvE1), Resolvin D1 (RvD1) and Resolvin D2 (RvD2) on dermal wound healing mechanism. In vitro migration assay studies performed using neutrophil cells confirmed the pro-resolution behavior of Resolvin compounds. All Resolvin compounds significantly blocked chemoattractant (fMLP) stimulated neutrophil migration. RvE1 demonstrated significantly better potency to block fMLP simulated neutrophil migration as compared to RvD1 and RvD2. This behavior was dose dependent and more pronounced at a concentration of 2000nM. Dorsal full thickness wound studies on wild type mice were performed using skin substitute (Integra Dermal Regenerative® Skin or Alloderm® Regenerative Tissue Matrix) along with administration of 2000nM Resolvin at the wound site. Results from the study revealed that complete wound closure time significantly reduced from 28.6±1.52 days (control) to 19.4±1.52 days with RvE1 treatment, 22.8±1.79 days with RvD2 treatment and 24.4±2.19 days with RvD1 treatment (n=5, p<0.05). Histology of wounds treated with RvE1 at Day 30 revealed a well-structured and repaired site with organized layers of dense collagen and a completely re-epithelized surface as compared to the saline treated wounds (control). These results demonstrate that the addition of Resolvins to a wound site significantly accelerates the wound healing and re-epithelialization process.