Modulation of Plet1 expression by N-Acetylglucosamine through the IL-17 A-MAPK pathway in an imiquimod-induced psoriasis mouse model.

Autor: Selvakumar B; Microbiota research group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates. bselvakumar@sharjah.ac.ae., Rah B; Iron Biology research Group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates., Jagal J; Drug Delivery research group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates., Sekar P; Microbiota research group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates., Moustafa R; Microbiota research group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates., Ramakrishnan RK; Tissue injury and repair research group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates., Haider M; Drug Delivery research group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates.; Department of Pharmaceutics and Pharmaceutical Technology, College of Pharmacy, University of Sharjah, Sharjah, 27272, United Arab Emirates., Ibrahim SM; College of Medicine and Health Science Research, Khalifa University of Science and Technology, Abu Dhabi, 127788, United Arab Emirates.; Institute of Experimental Dermatology, University of Lübeck, 2562, Lübeck, Germany., Samsudin R; Microbiota research group, Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates.; College of Dental Medicine, University of sharjah, Sharjah, 27272, United Arab Emirates.
Jazyk: angličtina
Zdroj: Inflammation research : official journal of the European Histamine Research Society ... [et al.] [Inflamm Res] 2024 Dec; Vol. 73 (12), pp. 2217-2230. Date of Electronic Publication: 2024 Oct 15.
DOI: 10.1007/s00011-024-01958-6
Abstrakt: Psoriasis (Ps) is a chronic inflammatory disorder marked by skin plaque formation, driven by immune dysregulation and genetic factors. Despite the available treatments, incidence of Ps is increasing in the dermatology patients. Novel strategies are crucial due to current treatment limitations. The interleukin 17 (IL-17) pathway is pivotal in Ps pathogenesis, however the expression of its putative target gene placenta expressed transcript 1 (Plet1) remains unstudied in Ps. Considering the potential anti-inflammatory properties of N-Acetylglucosamine (GlcNAc), our study explored its role in modulating Plet1 expression in an imiquimod (IMQ)-induced Ps mouse model. Our data demonstarted a significant reduction of inflammation and Psoriasis Area and Severity Index (PASI) scores, downregulation of growth factors (GFs), IL-17 A, and MAPK expression after GlcNAc treatment. In addition, GlcNAc treatment reduced neutrophils, monocyte-dendritic cells (Mo-DC) and conventional T cells (Tcons) while increasing monocyte-macrophages (Mo-Macs) and regulatory T cells (Tregs). GlcNAc treatment also downregulated Plet1 overexpression in psoriatic mouse skin and in vitro, reduced proliferation and apoptosis in IL-17 A stimulated human dermal fibroblasts (HDF), along with IL-17 A and TGF-β mRNA expression. Together, these data suggest that, GlcNAc interferes with downstream mechanisms in IL-17 pathway and downregulating Plet1 expression, presenting a promising strategy for Ps treatment.
Competing Interests: Declarations. Competing interests: All the authors declare that they have no competing interests. Conflict of interest: All authors declare, no conflict of interest.
(© 2024. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)
Databáze: MEDLINE
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