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Division of Environmental Science, Forensic and Social Environmental Medicine, Graduate School of Medical Science; and
* Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, Kanazawa, Japan
1Correspondence: Division of Environmental Science, Forensic and Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University, 13–1 Takara-machi, 920-8640 Kanazawa, Japan. E-mail: ohshimat{at}med.kanazawa-u.ac.jp
To clarify biological roles of tumor necrosis factor receptor p55 (TNF-Rp55) -mediated signals in wound healing, skin excisions were prepared in BALB/c (WT) and TNF-Rp55-deficient (KO) mice. In WT mice, the wound area was reduced to 50% of the original area 6 days after injury, with angiogenesis and collagen accumulation. Histopathologically, reepithelialization rate was 
80% 6 days. Myeloperoxidase activity and macrophage recruitment were the most evident 1 and 6 days after injury, respectively. Gene expression of adhesion molecules, interleukin 1
(IL-1), IL-1ß, monocyte chemoattractant protein 1, macrophage inflammatory protein 1 (MIP-1), MIP-2, transforming growth factor ß1 (TGF-ß1) connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), Flt-1, and Flk-1 was enhanced at the wound site. In KO mice, an enhancement in angiogenesis, collagen content, and reepithelialization was accelerated with the increased gene expression of TGF-ß1, CTGF, VEGF, Flt-1, and Flk-1 at the wound sites, resulting in accelerated wound healing compared with WT mice. In contrast, leukocyte infiltration, mRNA expression of adhesion molecules, and cytokines were significantly reduced in KO mice. These observations suggest that TNF-Rp55-mediated signals have some role in promoting leukocyte infiltration at the wound site and negatively affect wound healing, probably by reducing angiogenesis and collagen accumulation.—Mori, R., Kondo, T., Ohshima, T., Ishida, Y., Mukaida, N. Accelerated wound healing in tumor necrosis factor receptor p55-deficient mice with reduced leukocyte infiltration.
Key Words: TNF-Rp55 • angiogenesis • collagen production
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