Endogenous IL-10 Contributes to Wound Healing and Regulates Tissue Repair

Abstract

AbstractBackgroundInterleukin-10 (IL-10) is essential in fetal regenerative wound healing and likewise promotes a regenerative phenotype in adult dermal wounds. However, the role of endogenous IL-10 in postnatal dermal wound healing is not well established. We sought to determine the role of IL-10 in murine full thickness, excisional wounds that are splinted to prevent contracture and mimic human patterns of wound closure.MethodsFull thickness, excisional wounds were made in wildtype (WT) and IL-10-/- mice on a C57BL/6J background (F/M, 8wks old). In a subset of wounds, contraction was prevented by splinting with silicone stents (stenting) and maintaining a moist wound microenvironment using a semi-occlusive dressing. Wounds were examined for re-epithelialization, granulation tissue deposition, and inflammatory cell infiltrate at day 7 and fibrosis and scarring at day 30 post-wounding.ResultsWe observed no difference in wound healing rate between WT and IL-10-/- mice in either the stented or unstented group. At day 7, unstented IL-10-/- wounds had a larger granulation tissue area and more inflammatory infiltrate than their WT counterparts. However, we did observe more F4/80+ cell infiltrate in stented IL-10-/- wounds at day 7. At day 30, stented wounds had increased scar area and epithelial thickness compared to unstented wounds.ConclusionsThese data suggest that endogenous IL-10 expression does not alter closure of full thickness excisional wounds when wound hydration and excessive contraction are controlled. However, the loss of IL-10 leads to increased inflammatory cell infiltration and scarring. These data suggest that previous reports of increased rates of healing in IL-10-/- mice ought to be revisited considering recent advances in wound healing models. Moreover, these new findings suggest that IL-10 contributes to regulation of inflammation without compromising the healing response.