Interferon-gamma inhibits healing post scald burn injury

Impaired healing after severe burns remains a reason for prolonged hospitalization, opportunistic infections, and debilitating scarring. Interferon-gamma (IFN-?) is an important immune regulator that has been shown to inhibit collagen synthesis by fibroblasts, resulting in delayed healing in incision wounds. To determine whether IFN-? plays similar roles in the healing process after severe burn, we induced scald injury in mice deficient or sufficient in IFN-? and examined local responses. In the absence of IFN-?, scalded areas healed faster. This was associated with attenuated local inflammatory responses, enhanced reepithelialization, increased proliferation of keratinocytes in reepithelialized leading edges, and up-regulation of growth factors in burned skin areas. Furthermore, angiogenesis and myofibroblast formation commenced and terminated earlier in IFN-?/ mice compared with wild type (WT) controls. Our observations demonstrate that inhibition of IFN-? results in accelerated healing after burn injury by dampening excessive inflammation and facilitating reepithelialization, collagen deposition, and wound contraction.