IL‐17A promotes neutrophilic inflammation and disturbs acute wound healing in skin

• DOI: 10.1111/exd.13115
• Publication Date: 2016-06-15T18:34:55Z
• Authors: Naoyuki Takagi; Kazuyoshi Kawakami; Emi Kanno; Hiromasa Tanno; Atsushi Takeda; Keiko Ishii; Yoshimichi Imai; Yoichiro Iwakura; Masahiro Tachi
• Keywords: Proinflammatory cytokine; Myofibroblast; Neutrophil elastase; Knockout mouse

Abstract In the wound healing process, neutrophils are first inflammatory cells to move tissues. They sterilize wounds by killing microbes, and they stimulate other immune protect host from infection. contrast, neutrophil‐derived proteases cause damage tissues, so play dual opposite roles in healing. Interleukin‐17A ( IL ‐17A) is a proinflammatory cytokine that promotes recruitment of these cells. The role this process not fully clarified. present study, therefore, we examined how defect ‐17A production affected skin. ‐17A‐knockout KO ) mice showed promoted closure, myofibroblast differentiation collagen deposition decreased neutrophil accumulation compared with wild‐type WT mice. administration recombinant led delayed low accelerated neutrophilic accumulation. addition, treatment ‐17A‐administered elastase inhibitor improved repair same level as These results indicated hampered suggested inflammation caused may be associated impaired