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Interferon-gamma inhibits healing post scald burn injury.

Authors
Type
Published Article
Journal
Wound Repair and Regeneration
Publisher
Wiley (Blackwell Publishing)
Volume
20
Issue
4
Pages
580–580
Identifiers
DOI: 10.1111/j.1524-475X.2012.00812.x
Source
Soulika Lab - UC Davis dermatology-ucdavis
License
Unknown

Abstract

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.

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