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Special Issue "Therapy and Prevention of Atopic Dermatitis and Psoriasis 2020"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2020.

Special Issue Editors

Prof. Dr. Masutaka Furue
Website
Guest Editor
Chair, Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan
Interests: atopic dermatitis; psoriasis; dioxin; aryl hydrocarbon receptor; skin neoplasms; melanoma; skin barrier; pruritus
Special Issues and Collections in MDPI journals
Assoc. Prof. Dr. Takeshi Nakahara
Website
Co-Guest Editor
Division of Skin Surface Sensing, Department of Dermatology, Kyushu University, Fukuoka, 812-8582, Japan
Interests: atopic dermatitis; urticaria; psoriasis; dendritic cells; itch
Assoc. Prof. Dr. Gaku Tsuji
Website
Co-Guest Editor
Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, Fukuoka, 812-8582, Japan
Interests: aryl hydrocarbon receptor; nuclear factor erythroid 2-related factor 2; oxidative stress; psoriasis; atopic dermatitis

Special Issue Information

Dear Colleagues,

The skin is the outermost part of the body and is an area where various external and internal stimuli interact. Complex interface reactions are necessary for maintaining the homeostasis of the epidermal and dermal compartments, and imbalance results in numerous inflammatory disorders, such as psoriasis and atopic dermatitis. The excellent therapeutic success of biological treatments stress the pathogenetic importance of the TNF-α/IL-23/IL-17 axis for psoriasis and IL-4/IL-13 signals for atopic dermatitis. Common external stimuli include ultraviolet rays, chemicals, allergens, and environmental pollutants. Some of these agents modulate psoriatic and atopic inflammation by activating the oxidative aryl hydrocarbon receptor as well as the antioxidative NRF2 transcription factors. Various cytochemokines involved in Th17 and Th2 deviation are also involved in psoriatic and atopic inflammation, respectively, by facilitating the differentiation and recruitent of pathogenic dendritic cells, T-cells, and innate lymphoid cells.

In this Special Issue of IJMS, we will publish cutting-edge information regarding skin inflammation, therapy, and prevention, especially related to psoriatic and atopic inflammation. We warmly welcome submissions, including original papers and reviews.

Prof. Dr. Masutaka Furue
Assoc. Prof. Dr. Takeshi Nakahara
Assoc. Prof. Dr. Gaku Tsuji
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammatory skin diseases;
  • psoriasis;
  •  atopic dermatitis;
  • environmental pollutants;
  • aryl hydrocarbon receptor;
  • NRF2

Published Papers (3 papers)

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Research

Open AccessArticle
Skin Mycobiome of Psoriasis Patients is Retained during Treatment with TNF and IL-17 Inhibitors
Int. J. Mol. Sci. 2020, 21(11), 3892; https://doi.org/10.3390/ijms21113892 - 29 May 2020
Abstract
Background: Biological treatment relieves refractory skin lesions in patients with psoriasis; however, changes in the fungal microbiome (the mycobiome) on the skin are unclear. Methods: The skin mycobiome of psoriasis patients treated with TNF inhibitors (TNFi, n = 5) and IL-17 inhibitors (IL-17i, [...] Read more.
Background: Biological treatment relieves refractory skin lesions in patients with psoriasis; however, changes in the fungal microbiome (the mycobiome) on the skin are unclear. Methods: The skin mycobiome of psoriasis patients treated with TNF inhibitors (TNFi, n = 5) and IL-17 inhibitors (IL-17i, n = 7) was compared with that of patients not receiving systemic therapy (n = 7). Skin swab samples were collected from non-lesional post-auricular areas. Fungal DNA was sequenced by ITS1 metagenomic analysis and taxonomic classification was performed. Results: An average of 37543 reads/sample were analyzed and fungi belonging to 31 genera were detected. The genus Malassezia accounted for >90% of reads in 7/7 samples from the no-therapy group, 4/5 from the TNFi group, and 5/7 from the IL-17i group. Biodiversity was low in those three groups. Few members of the genus trichophyton were detected; the genus Candida was not detected at all. Among the Malassezia species, M. restricta was the major species in 6/7 samples from the no-therapy group, 4/5 from the TNFi group, and 5/7 from the IL-17i group whose the other largest species revealed M. globosa. Conclusions: The mycobiome is retained on post-auricular skin during systemic treatment with TNF and IL-17 inhibitors. Full article
(This article belongs to the Special Issue Therapy and Prevention of Atopic Dermatitis and Psoriasis 2020)
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Open AccessArticle
Exacerbated Imiquimod-Induced Psoriasis-Like Skin Inflammation in IRF5-Deficient Mice
Int. J. Mol. Sci. 2020, 21(10), 3681; https://doi.org/10.3390/ijms21103681 - 23 May 2020
Abstract
Interferon regulatory factors (IRFs) play diverse roles in the regulation of the innate and adaptive immune responses in various diseases. In psoriasis, IRF2 is known to be involved in pathogenesis, while studies on other IRFs are limited. In this study, we investigated the [...] Read more.
Interferon regulatory factors (IRFs) play diverse roles in the regulation of the innate and adaptive immune responses in various diseases. In psoriasis, IRF2 is known to be involved in pathogenesis, while studies on other IRFs are limited. In this study, we investigated the role of IRF5 in psoriasis using imiquimod-induced psoriasis-like dermatitis. Although IRF5 is known to play a critical role in the induction of proinflammatory cytokines by immune cells, such as dendritic cells (DCs), macrophages, and monocytes, IRF5 deficiency unexpectedly exacerbated psoriasiform skin inflammation. The interferon-α and tumor necrosis factor-α mRNA expression levels were decreased, while levels of Th17 cytokines including IL-17, IL-22, and IL-23 were increased in IRF5-deficient mice. Furthermore, IL-23 expression in DCs from IRF5-deficient mice was upregulated both in steady state and after toll-like receptor 7/8 agonist stimulation. Importantly, the expression of IRF4, which is also important for the IL-23 production in DCs, was augmented in DCs from IRF5-deficient mice. Taken together, our results suggest that IRF5 deficiency induces the upregulation of IRF4 in DCs followed by augmented IL-23 production, resulting in the amplification of Th17 responses and the exacerbation of imiquimod-induced psoriasis-like skin inflammation. The regulation of IRF4 or IRF5 expression may be a novel therapeutic approach to psoriasis. Full article
(This article belongs to the Special Issue Therapy and Prevention of Atopic Dermatitis and Psoriasis 2020)
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Open AccessArticle
Inflammatory Skin-Derived Cytokines Accelerate Osteoporosis in Mice with Persistent Skin Inflammation
Int. J. Mol. Sci. 2020, 21(10), 3620; https://doi.org/10.3390/ijms21103620 - 20 May 2020
Abstract
Secondary osteoporosis can also be caused by chronic inflammatory skin disease as well as rheumatoid arthritis or inflammatory bowel disease. However, the exact role of osteoporosis in inflammatory skin conditions has not been elucidated. Using a mouse model of dermatitis, we investigated the [...] Read more.
Secondary osteoporosis can also be caused by chronic inflammatory skin disease as well as rheumatoid arthritis or inflammatory bowel disease. However, the exact role of osteoporosis in inflammatory skin conditions has not been elucidated. Using a mouse model of dermatitis, we investigated the pathophysiology of osteoporosis in inflammatory skin conditions and the therapeutic impact of osteoporosis medication on inflammatory skin disease. We employed model mice of spontaneous skin inflammation, specifically overexpressing human caspase-1 in the epidermis. Bone density and the expression of various mRNAs in the femur were examined by micro CT and RT-PCR. The effects of minodronate and anti-RANKL antibody on bone structure, histology, and femur blood flow were studied. The mouse model of skin inflammation showed a marked decrease in bone density compared to wild-type littermates with abnormalities in both bone resorption and formation. Minodronate improved bone density by decreasing osteoclasts, but anti-RANKL antibody did not improve. In the dermatitis model, the blood flow in the bone marrow was decreased, and minodronate restored this parameter. A model of persistent dermatitis exhibited marked osteoporosis, but the impact of chronic dermatitis on osteoporosis has not been thoroughly investigated. We should explore the pathogenesis of osteoporosis in skin inflammatory diseases. Full article
(This article belongs to the Special Issue Therapy and Prevention of Atopic Dermatitis and Psoriasis 2020)
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