BACKGROUND: 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. OBJECTIVE: We aimed to ascertain the role of neuropeptides secreted from neurons in the pathogenesis of psoriasis in vivo. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: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. OBJECTIVE: We aimed to ascertain the role of neuropeptides secreted from neurons in the pathogenesis of psoriasis in vivo. METHODS: The release of neuropeptide was inhibited by injecting Botulinum toxin B (BTX-B) on Imiquimod (IMQ)-induced psoriasis-like dermatitismice 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. RESULTS: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. CONCLUSION: 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.
Authors: Wanhong Ding; Lori L Stohl; Jad Saab; Shayan Azizi; Xi K Zhou; Devina Mehta; Richard D Granstein Journal: J Immunol Date: 2022-01-14 Impact factor: 5.422
Authors: Marius Nicolae Popescu; Cristina Beiu; Mădălina Gabriela Iliescu; Mara Mădălina Mihai; Liliana Gabriela Popa; Ana Maria Alexandra Stănescu; Mihai Berteanu Journal: Medicina (Kaunas) Date: 2022-06-16 Impact factor: 2.948
Authors: Mi Ran Choi; Hae Dong Kim; Sinyoung Cho; Seong Ho Jeon; Dong Hyun Kim; Jungwon Wee; Young Duk Yang Journal: Int J Mol Sci Date: 2021-07-01 Impact factor: 5.923