Fetal wound repair results in scar formation in interleukin-10-deficient mice in a syngeneic murine model of scarless fetal wound repair

Background: Fetal dermal wound healing is characterized by minimal inflamma tion, restoration of normal dermal architecture, and scarless repair. The a uthors have shown that proinflammatory cytokines interleukin-6 (IL-6) and i nterleukin-8 (IL-8) are diminished during fetal wound repair. Interleukin-1 0 (IL-10) is an antiinflammatory cytokine that decreases production of IL-6 and IL-8. The authors hypothesized that diminished IL-6 and IL-8 and minim al inflammation may be caused by IL-10. Methods: To test this hypothesis, the authors developed a new syngeneic mur ine model of fetal wound repair in which 15-day-gestation skin from either normal C57BL/6 or transgenic C57BL/6 IL-10 knockout mice was grafted to the hack of the same strain adult mice. The grafts were incisionally wounded a fter 5 days, harvested at 1 week, and analyzed for inflammatory response an d scar formation. Results: Wounds in normal fetal skin grafts showed minimal inflammation and normal dermal reticular collagen pattern at the site of the wound, consist ent with scarless repair. In contrast, wounds in IL-10 knockout fetal skin grafts showed significant inflammation and scar formation. Conclusions: Fetal skin grafts on adult syngeneic mice heal without inflamm ation or scar formation. The absence of IL-10 in fetal skin results in scar formation, intrinsic lack of IL-10 may result in continued amplification o f the inflammatory cytokine cascade, continued stimulation of fibroblasts, and abnormal collagen deposition. IL-10 is necessary for scarless wound rep air to occur. Copyright (C) 2000 by W.B. Saunders Company.