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-γ) 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-γ plays similar roles in the healing process after severe burn, we induced scald injury in mice deficient or sufficient in IFN-γ and examined local responses. In the absence of IFN-γ, 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-γ(-/-)  mice compared with wild type (WT) controls. Our observations demonstrate that inhibition of IFN-γ results in accelerated healing after burn injury by dampening excessive inflammation and facilitating reepithelialization, collagen deposition, and wound contraction.
Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children-Northern California, Sacramento, California 95817, USA.
Haitao
H
Shen
Pamela
P
Yao
Eunyoung
E
Lee
David
D
Greenhalgh
Athena M
AM
Soulika
D000818:Animals; D002056:Burns / Q000276:immunology / Q000473:pathology*; D049109:Cell Proliferation; D003094:Collagen / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000172:deficiency / Q000378:metabolism*; D015603:Keratinocytes / Q000276:immunology / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D014945:Wound Healing / Q000276:immunology
D007371:Interferon-gamma; D003094:Collagen