TY - JOUR
T1 - Distinct Roles for Dectin-1 and Dectin-2 in Skin Wound Healing and Neutrophilic Inflammatory Responses
AU - Yamaguchi, Kenji
AU - Kanno, Emi
AU - Tanno, Hiromasa
AU - Sasaki, Ayako
AU - Kitai, Yuki
AU - Miura, Takayuki
AU - Takagi, Naoyuki
AU - Shoji, Miki
AU - Kasamatsu, Jun
AU - Sato, Ko
AU - Sato, Yuka
AU - Niiyama, Momoko
AU - Goto, Yuka
AU - Ishii, Keiko
AU - Imai, Yoshimichi
AU - Saijo, Shinobu
AU - Iwakura, Yoichiro
AU - Tachi, Masahiro
AU - Kawakami, Kazuyoshi
N1 - Funding Information:
We thank Dr Sho Yamasaki (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan) for providing us with Dectin-1 and Dectin-2 reporter cells and Dr Hiromitsu Hara (Department of Immunology, Graduate School of Medical and Dental Sciences, Kagoshima University, Japan) for providing us with the CARD9KO mice. This work was supported in part by a Grant-in-Aid for Scientific Research (C) (18K09473), Grant-in-Aid for Scientific Research (B) (19H03812), a Grant-in-Aid for Challenging Exploratory Research (19K22649), and a Grant-in-Aid for Young Scientists (19K19494) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
Funding Information:
We thank Dr Sho Yamasaki (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan) for providing us with Dectin-1 and Dectin-2 reporter cells and Dr Hiromitsu Hara (Department of Immunology, Graduate School of Medical and Dental Sciences, Kagoshima University, Japan) for providing us with the CARD9KO mice. This work was supported in part by a Grant-in-Aid for Scientific Research (C) (18K09473), Grant-in-Aid for Scientific Research (B) (19H03812), a Grant-in-Aid for Challenging Exploratory Research (19K22649), and a Grant-in-Aid for Young Scientists (19K19494) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. Conceptualization: KY, EK, MT, KK; Data Curation: KY, EK, HT, KK; Formal, Analysis: KY, EK, HT, AS, YK; Funding Acquisition: EK, MT, KK; Investigation: KY, HT, TM, NT, MS, JK, KS, YS, MN, YG, KI; Methodology: KY, HT, JK, KS, YI; Project Administration: KY, EK, KK; Resources: KY, EK, HT, SS, YI, KK; Supervision: EK, MT, KK; Validation: KY, EK, HT, KK; Visualization: KY, EK, MT, KK; Writing - Original, Draft Preparation: KY, EK, KK; Writing - Review and Editing: KY, EK, KK
Publisher Copyright:
© 2020 The Authors
PY - 2021/1
Y1 - 2021/1
N2 - C-type lectin receptors recognize microbial polysaccharides. The C-type lectin receptors such as dendritic cell-associated C-type lectin (Dectin)-1 and Dectin-2, which are triggered by β-glucan and α-mannan, respectively, contribute to upregulation of the inflammatory response. Recently, we demonstrated that activation of the Dectin-2 signal delayed wound healing; in previous studies, triggering the Dectin-1 signal promoted this response. However, the precise roles of these C-type lectin receptors in skin wound healing remain unclear. This study was conducted to determine the roles of Dectin-1 and Dectin-2 in skin wound healing, with a particular focus on the kinetics of neutrophilic inflammatory response. Full-thickness wounds were created on the backs of C57BL/6 mice, and the effects of Dectin-1 or Dectin-2 deficiency and those of β-glucan or α-mannan administration were examined. We also analyzed wound closure, histological findings, and neutrophilic inflammatory response, including neutrophil extracellular trap formation at the wound sites. We found that Dectin-1 contributed to the acceleration of wound healing by inducing early-phase neutrophil accumulation, whereas Dectin-2 was involved in prolonged neutrophilic responses and neutrophil extracellular trap formation, leading to delayed wound healing. Dectin-2 deficiency also improved collagen deposition and TGF-β1 expression. These results suggest that Dectin-1 and Dectin-2 have different roles in wound healing through their different effects on the neutrophilic response.
AB - C-type lectin receptors recognize microbial polysaccharides. The C-type lectin receptors such as dendritic cell-associated C-type lectin (Dectin)-1 and Dectin-2, which are triggered by β-glucan and α-mannan, respectively, contribute to upregulation of the inflammatory response. Recently, we demonstrated that activation of the Dectin-2 signal delayed wound healing; in previous studies, triggering the Dectin-1 signal promoted this response. However, the precise roles of these C-type lectin receptors in skin wound healing remain unclear. This study was conducted to determine the roles of Dectin-1 and Dectin-2 in skin wound healing, with a particular focus on the kinetics of neutrophilic inflammatory response. Full-thickness wounds were created on the backs of C57BL/6 mice, and the effects of Dectin-1 or Dectin-2 deficiency and those of β-glucan or α-mannan administration were examined. We also analyzed wound closure, histological findings, and neutrophilic inflammatory response, including neutrophil extracellular trap formation at the wound sites. We found that Dectin-1 contributed to the acceleration of wound healing by inducing early-phase neutrophil accumulation, whereas Dectin-2 was involved in prolonged neutrophilic responses and neutrophil extracellular trap formation, leading to delayed wound healing. Dectin-2 deficiency also improved collagen deposition and TGF-β1 expression. These results suggest that Dectin-1 and Dectin-2 have different roles in wound healing through their different effects on the neutrophilic response.
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U2 - 10.1016/j.jid.2020.04.030
DO - 10.1016/j.jid.2020.04.030
M3 - Article
C2 - 32511980
AN - SCOPUS:85087929842
VL - 141
SP - 164-176.e8
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
SN - 0022-202X
IS - 1
ER -