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      Chemical Composition and Inhibitory Effect of Lentinula edodes Ethanolic Extract on Experimentally Induced Atopic Dermatitis in Vitro and in Vivo

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          Abstract

          The ethanolic extract of Lentinula edodes was partially analyzed and then characterized for its efficacy in treating atopic dermatitis. Polyphenols were determined to be the major antioxidant component in the extract (6.12 mg/g), followed by flavonoids (1.76 mg/g), β-carotene (28.75 μg/g), and lycopene (5.25 μg/g). An atopic dermatitis (AD) model was established and epidermal and dermal ear thickness, mast cell infiltration, and serum immunoglobulin levels were measured after oral administration of the L. edodes extract for 4 weeks. L. edodes extract decreased Dermatophagoides farinae extract (DFE) and 4-dinitrochlorobenzene (DNCB)-induced expression of several inflammatory cytokines in the ears, cervical lymph nodes, and splenocytes. Consequently, L. edodes extract may have therapeutic potential in the treatment of AD attributable to its immunomodulatory effects.

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          Production of interleukin 22 but not interleukin 17 by a subset of human skin-homing memory T cells.

          Thomas Duhen, Rebekka Geiger, David Jarrossay … (2009)
          Interleukin 22 (IL-22) is a cytokine produced by the T(H)-17 lineage of helper T cells and NK-22 subset of natural killer cells that acts on epithelial cells and keratinocytes and has been linked to skin homeostasis and inflammation. Here we characterize a population of human skin-homing memory CD4(+) T cells that expressed the chemokine receptors CCR10, CCR6 and CCR4 and produced IL-22 but neither IL-17 nor interferon-gamma (IFN-gamma). Clones isolated from this population produced IL-22 only and had low or undetectable expression of the T(H)-17 and T helper type 1 (T(H)1) transcription factors RORgammat and T-bet. The differentiation of T cells producing only IL-22 was efficiently induced in naive T cells by plasmacytoid dendritic cells in an IL-6- and tumor necrosis factor-dependent way. Our findings delineate a previously unknown subset of human CD4(+) effector T cells dedicated to skin pathophysiology.
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            Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling.

            Stefanie Eyerich, Kilian Eyerich, Davide Pennino … (2009)
            Th subsets are defined according to their production of lineage-indicating cytokines and functions. In this study, we have identified a subset of human Th cells that infiltrates the epidermis in individuals with inflammatory skin disorders and is characterized by the secretion of IL-22 and TNF-alpha, but not IFN-gamma, IL-4, or IL-17. In analogy to the Th17 subset, cells with this cytokine profile have been named the Th22 subset. Th22 clones derived from patients with psoriasis were stable in culture and exhibited a transcriptome profile clearly separate from those of Th1, Th2, and Th17 cells; it included genes encoding proteins involved in tissue remodeling, such as FGFs, and chemokines involved in angiogenesis and fibrosis. Primary human keratinocytes exposed to Th22 supernatants expressed a transcriptome response profile that included genes involved in innate immune pathways and the induction and modulation of adaptive immunity. These proinflammatory Th22 responses were synergistically dependent on IL-22 and TNF-alpha. Furthermore, Th22 supernatants enhanced wound healing in an in vitro injury model, which was exclusively dependent on IL-22. In conclusion, the human Th22 subset may represent a separate T cell subset with a distinct identity with respect to gene expression and function, present within the epidermal layer in inflammatory skin diseases. Future strategies directed against the Th22 subset may be of value in chronic inflammatory skin disorders.
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              Th2 Cytokines and Atopic Dermatitis.

              Eric B Brandt, Umasundari Sivaprasad (2011)
              Atopic dermatitis (AD), a chronic relapsing inflammatory skin disease, is increasing in prevalence around the world. Intensive research is ongoing to understand the mechanisms involved in the development of AD and offer new treatment options for patients suffering from AD. In this review, we highlight the importance of allergic Th2 responses in the development of the disease and summarize relevant literature, including genetic studies, studies of human skin and mechanistic studies on keratinocytes and mouse models of AD. We discuss the importance of the skin barrier and review recent findings on the pro-Th2 cytokines TSLP, IL-25, and IL-33, notably their ability to polarize dendritic cells and promote Th2 responses. After a brief update on the contribution of different T-cell subsets to AD, we focus on Th2 cells and the respective contributions of each of the Th2 cytokines (IL-4, IL-13, IL-5, IL-31, and IL-10) to AD. We conclude with a brief discussion of the current gaps in our knowledge and technical limitations.
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                Author and article information

                Contributors
                Derek J. McPhee: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Molecules
                Journal ID (iso-abbrev): Molecules
                Journal ID (publisher-id): molecules
                Title: Molecules
                Publisher: MDPI
                ISSN (Electronic): 1420-3049
                Publication date (Electronic): 29 July 2016
                Publication date Collection: August 2016
                Volume: 21
                Issue: 8
                Electronic Location Identifier: 993
                Affiliations
                [1 ]Division of Sport Science, College of Science and Technology, Konkuk University, Chungju 27478, Korea; ooj7990@ 123456kku.ac.kr
                [2 ]School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology, Gwangju 61005, Korea
                [3 ]Division of Food Bioscience, College of Biomedical and Health Sciences, Konkuk University, Chungju 27478, Korea
                Author notes
                [* ]Correspondence: zeeyong@ 123456gist.ac.kr (Z.-Y.P.); eunkyungkim@ 123456kku.ac.kr (E.-K.K.); Tel.: +82-62-715-2496 (Z.-Y.P.); +82-43-840-3581 (E.-K.K.)
                Article
                Publisher ID: molecules-21-00993
                DOI: 10.3390/molecules21080993
                PMC ID: 6273379
                PubMed ID: 27483228
                SO-VID: 263bbaf3-435a-488d-be58-63a140409ae6
                Copyright © © 2016 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 May 2016
                Date accepted : 25 July 2016
                Categories
                Subject: Article

                Keywords: atopic dermatitis,lentinula edodes,immunomodulatory,inflammatory cytokines
                Data availability:
                Keywords: atopic dermatitis, lentinula edodes, immunomodulatory, inflammatory cytokines

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