ReferenceID 5467

Hyperforin Ameliorates Imiquimod-Induced Psoriasis-Like Murine Skin Inflammation by Modulating IL-17A-Producing γδ T Cells

Front Immunol

Hyperforin is a major active constituent of Hypericum perforatum L. extract, which is widely used for the treatment of depressive disorders. Recent studies have reported that hyperforin reduced inflammation in stroke and

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Reference Id
5467
Evidence Id
22057
Core Evidence Id
22057
Source Reference Id
4183
Herb2 Reference Id
HBREF004980
Subject Paper Key
HBIN029826_34025642
Pubmed Id
34025642
Doi
10.3389/fimmu.2021.635076
Paper Title
Hyperforin Ameliorates Imiquimod-Induced Psoriasis-Like Murine Skin Inflammation by Modulating IL-17A-Producing γδ T Cells
Paper Abstract
Hyperforin is a major active constituent of Hypericum perforatum L. extract, which is widely used for the treatment of depressive disorders. Recent studies have reported that hyperforin reduced inflammation in stroke and suppressed proliferation and differentiation in keratinocytes. Psoriasis is a chronic immune-mediated inflammatory skin disease in which the IL-23/IL-17 axis plays an important role. To investigate the underlying inflammatory mechanisms and response of hyperforin in psoriasis, we use imiquimod (IMQ)-induced mice model, in vitro cultured murine splenic gammadelta T cells, and HaCaT cells in this study. Data showed that hyperforin reduced epidermal thickness and decreased IMQ-induced pathological scores of cutaneous skin lesions in mice. Meanwhile we proved that hyperforin suppressed infiltration of CD3+ T cells and downregulated expression of Il1, Il6, Il23, Il17a, Il22, antimicrobial peptides (AMPs) in the skin lesion. Hyperforin significantly inhibited imiquimod-induced splenomegaly, reduced serum levels of TNF-alpha and IL-6, and IL-17A in splenocytes and draining lymph nodes. Our study also suggested that hyperforin lessened the infiltration of gammadelta T cell and CCR6+ gammadelta T cells in spleen and lymph nodes. Hyperforin also suppressed the typical psoriasis-like inflammatory responses and the infiltration of IL-17A+ cells in dermal gammadelta T cells of IMQ treated Tcrd -/- mice transferred with gammadelta T cells. In vitro studies, hyperforin reduced the expression and secretion of IL-17A in gammadelta T cells, and suppressed the activation of MAPK/STAT3 pathways in human keratinocyte HaCaT cells and gammadelta T cells. In conclusion, hyperforin alleviates IMQ-induced inflammation in psoriasis through suppressing the immune responses exerted by IL-17 A-producing gammadelta T cells and related cytokines by modulating MAPK/STAT3 pathways. Our study provided a novel therapeutic tragedy for psoriasis by which hyperforin attenuates psoriasis-related inflammatory responses.
Journal
Front Immunol
Publish Year
2021
Experiment Subject
mouse; human; hacat cells; human keratinocyte hacat cells; in vitro cultured murine splenic gammadelta t cells
Experiment Type
Animal & Cell Experiment
Phenotype Related
Stroke; Psoriasis; Depressive Disorders; Cutaneous Skin Lesions; Chronic Immune-mediated Inflammatory Skin Disease; Imiquimod-induced Splenomegaly; Imiquimod
Paper Title Cn
Paper Title En
Hyperforin Ameliorates Imiquimod-Induced Psoriasis-Like Murine Skin Inflammation by Modulating IL-17A-Producing γδ T Cells
Bilingual Status
semi_complete