Orf virus IL-10 accelerates wound healing while limiting inflammation and scarring

Interleukin (IL)‐10 plays a critical role in controlling wound inflammation and scar formation. Orf virus, a zoonotic parapoxvirus, induces proliferative skin lesions that resolve with minimal scarring. Orf virus encodes a range of factors that subvert the host's response to infection, including a homolog of IL‐10. This study investigated, using a murine full‐thickness wound model, whether purified orf virus IL‐10 (ovIL‐10) can regulate skin repair and scarring. Repeat injections of ovIL‐10 into wounded skin accelerated wound closure. Histological analyses of wound sections revealed that treatment with ovIL‐10 accelerated wound reepithelialization, granulation tissue coverage of the wound bed, and improved wound revascularization. In addition, wounds treated with ovIL‐10 showed a reduction in macrophage infiltration, myofibroblast differentiation, and wound contraction. Treatment of wounds with ovIL‐10 also resulted in a reduction in visible scarring that was consistent with the extent of scar tissue formed. Quantitative polymerase chain reaction analysis confirmed that ovIL‐10 reduced the expression of key mediators of inflammation and granulation tissue formation. These findings show that ovIL‐10, like mammalian IL‐10, limits inflammation and scar tissue formation and reveal a new role for both mammalian and viral IL‐10 in mediating tissue repair.