Dermatology

渡邊 総一郎

soichiro watanabe

基本情報

所属
藤田医科大学 医学部 医学科 皮膚科学 講師
学位
医学博士(2021年9月 藤田医科大学 医学部 医学科)

J-GLOBAL ID
201501009528048939
researchmap会員ID
7000012851

経歴

 6

学歴

 2

委員歴

 1

論文

 24
  • 湯浅 智子, 渡邊 総一郎, 秋田 浩孝, 浦野 誠, 岩月 啓氏, 岩田 洋平, 杉浦 一充
    日本皮膚科学会雑誌 134(4) 816-816 2024年4月  
  • Yurie Hasegawa, Yohei Iwata, Hidehiko Fukushima, Yoshihito Tanaka, Soichiro Watanabe, Kenta Saito, Hiroyuki Ito, Mizuki Sugiura, Masashi Akiyama, Kazumitsu Sugiura
    Scientific reports 12(1) 13384-13384 2022年8月4日  
    Loss-of-function homozygous or compound heterozygous mutations in IL36RN, which encodes interleukin-36 receptor antagonist (IL-36Ra), have been implicated in the pathogenesis of skin disorders. We previously reported that Il36rn-/- mice exhibit an enhanced contact hypersensitivity (CHS) response through increased neutrophil recruitment. In addition, Il36rn-/- mice show severe imiquimod-induced psoriatic skin lesions and enhanced neutrophil extracellular trap (NET) formation. We hypothesized that NETs may play an important role in the CHS response. To confirm this, we examined the CHS response and NET formation in Il36rn-/- mice. Il36rn-/- mice showed enhanced CHS responses, increased infiltration of inflammatory cells, including neutrophils, CD4+ T cells, and CD8+ T cells, NET formation, and enhanced mRNA expression of cytokines and chemokines, including IL-1β, C-X-C motif chemokine ligand (CXCL)1, CXCL2, and IL-36γ. Furthermore, NET formation blockade improved the CHS response, which consequently decreased inflammatory cell infiltration and NET formation. Consistently, we observed decreased expression of these cytokines and chemokines. These findings indicate that IL-36Ra deficiency aggravates the CHS response caused by excessive inflammatory cell recruitment, NET formation, and cytokine and chemokine production, and that NET formation blockade alleviates the CHS response. Thus, NET formation may play a prominent role in the CHS response.
  • Y Tanaka, Y Iwata, K Saito, H Fukushima, S Watanabe, Y Hasegawa, M Akiyama, K Sugiura
    Journal of the European Academy of Dermatology and Venereology : JEADV 36(2) 295-304 2022年2月  
    BACKGROUND: Loss-of-function homozygous or compound heterozygous mutations in IL36RN, which encodes interleukin-36 receptor antagonist (IL-36Ra), has been implicated in the pathogenesis of skin disorders. However, the pathogenic role of IL-36Ra in cutaneous ischemia-reperfusion (I/R) injury remains unclear. OBJECTIVES: We investigated the role of IL36Ra in cutaneous I/R injury. METHODS: We examined I/R injury in Il36rn-/- mice. The area of wounds, numbers of infiltrated cells, apoptotic cells and neutrophil extracellular trap (NET) formation were assessed. The expression levels of various genes were analysed using real-time RT-PCR. The expression of high mobility group box 1 (HMGB1), an endogenous toll-like receptor (TLR) 4 ligand, was confirmed using immunohistology, and serum HMGB1 levels were measured by ELISA. Cytokine production by stimulated cultured J774A.1 and HaCaT cells was examined. RESULTS: IL-36Ra deficiency resulted in significantly delayed wound healing and increased neutrophil and macrophage infiltration into the wound tissues. Il36rn-/- mice had increased mRNA expression levels of CXCL1, CXCL2, CCL4, TNF-α, TGF-β, IL-1β, IL-6 and IL-36γ relative to wild-type mice. Apoptosis was identified in keratinocytes by TUNEL assay. HMGB1 expression in the I/R site was decreased in both keratinocytes and adnexal cells, while serum HMGB1 levels were significantly elevated after reperfusion. The mRNA levels of various cytokines, including IL-1β, were elevated in J774A.1 cells through TLR4 signalling by HMGB1 stimulation. In addition, HaCaT cells stimulated with IL-1β showed significantly increased CXCL1, TNF-α, IL-6, IL-36β and IL-36γ mRNA expression. Furthermore, NET formation was increased by IL-36Ra deficiency. Finally, either the blockade of TLR4 signalling by TAK-242 or inhibition of NET formation by Cl-amidine normalized exacerbated I/R injury in Il36rn-/- mice. CONCLUSIONS: This study indicated that IL-36Ra deficiency exacerbates cutaneous I/R injury due to excessive inflammatory cell recruitment, NET formation, and excessive cytokine and chemokine production via the TLR4 pathway by HMGB1 released from epidermal apoptotic cells.
  • Soichiro Watanabe, Yohei Iwata, Kenta Saito, Kazumitsu Sugiura
    The Journal of Dermatology 49(1) e26-e27 2021年10月12日  査読有り筆頭著者
  • 小野田 裕子, 渡邊 総一郎, 岩田 洋平, 杉浦 一充, 蜂谷 芳可
    皮膚の科学 20(3) 258-258 2021年9月  

MISC

 66

主要な講演・口頭発表等

 3

担当経験のある科目(授業)

 1

共同研究・競争的資金等の研究課題

 1

その他

 1