IL-17A promotes neutrophilic inflammation and disturbs acute wound healing in skin.
In the wound healing process, neutrophils are the first inflammatory cells to move to the wound tissues. They sterilize wounds by killing microbes, and they stimulate other immune cells to protect the host from infection. In contrast, neutrophil-derived proteases cause damage to host tissues, so neutrophils play dual opposite roles in wound healing. Interleukin-17A (IL-17A) is a proinflammatory cytokine that promotes the recruitment of these cells. The role of this cytokine in the wound healing process is not fully clarified. In the present study, therefore, we examined how defect in IL-17A production affected the wound healing in skin. IL-17A-knockout (KO) mice showed promoted wound closure, myofibroblast differentiation and collagen deposition and decreased the neutrophil accumulation compared with wild-type (WT) mice. In contrast, the administration of recombinant IL-17A led to delayed wound closure, low collagen deposition and accelerated neutrophilic accumulation. In addition, the treatment of IL-17A-administered mice with a neutrophil elastase inhibitor improved the wound repair to the same level as that of WT mice. These results indicated that IL-17A hampered the wound healing process and suggested that neutrophilic inflammation caused by IL-17A may be associated with impaired wound healing in skin.
Department of Plastic and Reconstructive Surgery, Tohoku University, Sendai, Japan.
Naoyuki
N
Takagi
Department of Medical Microbiology, Mycology and Immunology, Tohoku University, Sendai, Japan.
Kazuyoshi
K
Kawakami
Department of Science of Nursing Practice, Tohoku University, Sendai, Japan.
Emi
E
Kanno
Department of Science of Nursing Practice, Tohoku University, Sendai, Japan.
Hiromasa
H
Tanno
Department of Plastic and Reconstructive Surgery, Tohoku University, Sendai, Japan.
Atsushi
A
Takeda
Department of Medical Microbiology, Mycology and Immunology, Tohoku University, Sendai, Japan.
Keiko
K
Ishii
Department of Plastic and Reconstructive Surgery, Tohoku University, Sendai, Japan.
Yoshimichi
Y
Imai
Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Yoichiro
Y
Iwakura
Department of Plastic and Reconstructive Surgery, Tohoku University, Sendai, Japan.
Masahiro
M
Tachi
D000818:Animals; D002454:Cell Differentiation / Q000235:genetics; D024042:Collagen Type I / Q000378:metabolism; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III / Q000378:metabolism; D005260:Female; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D020381:Interleukin-17 / Q000235:genetics* / Q000378:metabolism / Q000494:pharmacology; D007958:Leukocyte Count; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D058628:Myofibroblasts / Q000502:physiology; D009504:Neutrophils / Q000187:drug effects* / Q000473:pathology; D053491:Proteinase Inhibitory Proteins, Secretory / Q000494:pharmacology; D012879:Skin Physiological Phenomena; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects / Q000235:genetics*; D014950:Wounds, Penetrating / Q000378:metabolism* / Q000473:pathology
C000609875:COL3A1 protein, mouse; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D024061:Collagen Type III; C098680:Il17a protein, mouse; D020381:Interleukin-17; D053491:Proteinase Inhibitory Proteins, Secretory; D053773:Transforming Growth Factor beta1
IL-17A; neutrophil; wound healing