Essential involvement of IL-6 in the skin wound-healing process as evidenced by delayed wound healing in IL-6-deficient mice

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  • Zi-Qing Lin
    Department of Forensic & Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University , Japan
  • Toshikazu Kondo
    Department of Forensic & Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University , Japan
  • Yuko Ishida
    Department of Forensic & Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University , Japan
  • Tatsunori Takayasu
    Department of Forensic & Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University , Japan
  • Naofumi Mukaida
    Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University , Japan

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<jats:title>Abstract</jats:title> <jats:p>To clarify interleukin (IL)-6 roles in wound healing, we prepared skin excisions in wild-type (WT) and IL-6-deficient BALB/c [knockout (KO)] mice. In WT mice, the wound area was reduced to 50% of original size at 6 days after injury. Microscopically, leukocyte infiltration was evident at wound sites. Furthermore, the re-epithelialization rate was ∼80% at 6 days after injury with increases in angiogenesis and hydroxyproline contents. The gene expression of IL-1, chemokines, adhesion molecules, transforming growth factor-β1, and vascular endothelial growth factor was enhanced at the wound sites. In contrast, the enhanced expression of these genes was significantly reduced in KO mice. Moreover, in KO mice, the reduction of wound area was delayed with attenuated leukocyte infiltration, re-epithelialization, angiogenesis, and collagen accumulation. Finally, the administration of a neutralizing anti-IL-6 monoclonal antibody significantly delayed wound closure in WT mice. These observations suggest that IL-6 has crucial roles in wound healing, probably by regulating leukocyte infiltration, angiogenesis, and collagen accumulation.</jats:p>

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