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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 incisi...

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Published in:Wound Repair & Regeneration Vol. 20; no. 4; pp. 580 - 592
Main Authors: Shen, Haitao, Yao, Pamela, Lee, Eunyoung, Greenhalgh, David, Soulika, Athena M.
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell Jul/Aug2012
Online Access:View this record in EBSCOhost
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1111/j.1524-475X.2012.00812.x
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        atl: Interferon-gamma inhibits healing post scald burn injury.
      aug:
        au:
          Shen, Haitao
          Yao, Pamela
          Lee, Eunyoung
          Greenhalgh, David
          Soulika, Athena M.
        affil: Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children-Northern California; Department of Dermatology, School of Medicine, University of California, Davis
      sug:
        subj:
          Burns Prognosis
          Wound Healing Physiology
          Interferons Metabolism
          Animal Studies
          Mice
          Models, Biological
          Funding Source
          Skin Physiology
          Immunohistochemistry
          Flow Cytometry
          RNA Analysis
          Polymerase Chain Reaction
          Enzyme-Linked Immunosorbent Assay
          Data Analysis Software
          Analysis of Variance
          Mann-Whitney U Test
      ab: 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.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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