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Essential involvement of IL‐6 in the skin wound‐healing process as evidenced by delayed wound healing in IL‐6‐deficient mice
Author(s) -
Lin ZiQing,
Kondo Toshikazu,
Ishida Yuko,
Takayasu Tatsunori,
Mukaida Naofumi
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0802397
Subject(s) - wound healing , angiogenesis , hydroxyproline , chemokine , infiltration (hvac) , neovascularization , biology , immunology , interleukin , inflammation , cancer research , cytokine , endocrinology , physics , thermodynamics
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.