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Interferon-gamma inhibits healing post scald burn injury

Authors

  • Haitao Shen PhD,

    1. Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children—Northern California, Sacramento, California
    2. Department of Dermatology, School of Medicine, University of California, Davis, Sacramento, California
    Current affiliation:
    1. Laboratory of Pathology, Hebei Medical University, Shijiazhuang, China
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  • Pamela Yao BS,

    1. Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children—Northern California, Sacramento, California
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  • Eunyoung Lee PhD,

    1. Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children—Northern California, Sacramento, California
    2. Department of Dermatology, School of Medicine, University of California, Davis, Sacramento, California
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  • David Greenhalgh MD,

    1. Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children—Northern California, Sacramento, California
    2. Department of Surgery, School of Medicine, University of California, Davis, Sacramento, California
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  • Athena M. Soulika PhD

    Corresponding author
    1. Department of Dermatology, School of Medicine, University of California, Davis, Sacramento, California
    • Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children—Northern California, Sacramento, California
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  • All authors’ address: Shriners Hospital, Sacramento, California.

Reprint requests:

Dr. Athena M. Soulika, UC Davis School of Medicine, c/o Shriners Hospital, 2425 Stockton Blvd., Sacramento, CA 95817.

Tel: +1 916-453-5061;

Fax: +1 916-453-2288;

Email: athena.soulika@ucdmc.ucdavis.edu

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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