Suppression of neuropeptide by botulinum toxin improves imiquimod-induced psoriasis-like dermatitis via the regulation of neuroimmune system

•BTX-B suppresses the progression of psoriasis-like dermatitis in IMQ-treated mice.•BTX-B suppressed the type 17 inflammation in IMQ-treated skin lesions.•BTX-B regulates psoriasis via neuroimmune system.•Neuropeptide inhibitor, including BTX can be applied to the treatment of psoriasis. Psoriasis i...

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Veröffentlicht in:Journal of dermatological science 2021-01, Vol.101 (1), p.58-68
Hauptverfasser: Amalia, Syahla Nisaa, Uchiyama, Akihiko, Baral, Hritu, Inoue, Yuta, Yamazaki, Sahori, Fujiwara, Chisako, Sekiguchi, Akiko, Yokoyama, Yoko, Ogino, Sachiko, Torii, Ryoko, Hosoi, Mari, Ishikawa, Osamu, Motegi, Sei-ichiro
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Sprache:eng
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Zusammenfassung:•BTX-B suppresses the progression of psoriasis-like dermatitis in IMQ-treated mice.•BTX-B suppressed the type 17 inflammation in IMQ-treated skin lesions.•BTX-B regulates psoriasis via neuroimmune system.•Neuropeptide inhibitor, including BTX can be applied to the treatment of psoriasis. Psoriasis is a multifactorial disease arises from a complex interaction of genetics, immune system, and environmental aspects. IL-23/Th17 immune axis has been considered as a primary modulator in psoriasis. In addition, several findings imply that nervous system may take a part in the pathogenesis of psoriasis, suggesting that nervous system, through its neuropeptide, may interact with immune system and lead to the formation of psoriasis. We aimed to ascertain the role of neuropeptides secreted from neurons in the pathogenesis of psoriasis in vivo. The release of neuropeptide was inhibited by injecting Botulinum toxin B (BTX-B) on Imiquimod (IMQ)-induced psoriasis-like dermatitis mice model. Quantification of skin dermatitis, infiltrating inflammatory cells, and the production of cytokines at the lesional skin area were performed by PSI score, immunostaining, and real-time PCR. We also tested the effect of selective CGRP antagonist (CGRP8−37) on psoriasis-like dermatitis in IMQ-treated mice. BTX-B injection significantly suppressed PSI score and reduced the number of CD4+ T cells, CD11c+ dendritic cells, and the production of IL-17A/F in the lesional skin. The expressions of PGP9.5+ nerve fibers and neuropeptides (SP, CGRP) were also significantly reduced following BTX-B injection. Additionally, CGRP antagonist also suppressed the development of IMQ-induced psoriasis-like dermatitis in mice. The suppression of neuropeptide secretion in the skin by BTX injection might inhibit nerve elongation, the infiltration of immune cells, as well as IL-17 production, resulting in the improvement of psoriasis. Neuropeptide inhibitor could also be applied to the treatment of psoriasis.
ISSN:0923-1811
1873-569X
DOI:10.1016/j.jdermsci.2020.11.003