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Progress in the Pathogenesis and Therapeutics of Psoriasis

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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: closed (31 August 2023) | Viewed by 13538

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Prof. Dr. Naoko Kanda

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Department of Dermatology, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Chiba, Japan
Interests: psoriasis; atopic dermatitis; cutaneous immunology; cytokines; chemokines; keratinocytes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Psoriasis is a chronic inflammatory skin disease characterized by scaly indurated erythema, IL-17-skewed abnormal immunity, and the aberrant differentiation as well as hyperproliferation of epidermal keratinocytes. Patients with psoriasis are associated with arthritis, diabetes, or cardiovascular diseases. The tumor necrosis factor-alpha/IL-23/IL-17 axis is the mainstay of its pathogenesis; however, other pathways are also involved, such as the abnormal regulation of regulatory T cells, resident memory T cells, or gut microbiota. In recent years, many breakthroughs have occurred in the research on psoriasis. The clarification of pathogenesis produced target therapy such as biologics, while the research on therapeutic efficacy generated novel findings in pathomechamistic studies. Furthermore, the viewpoints of the research are affected by recent dynamic environmental changes, such as the SARS-CoV-2 epidemic.

This Special Issue aims to provide a platform for molecular mechanistic research on psoriasis with a special focus on potential treatments and novel pathogenic pathways involved in this disease. We warmly welcome your submissions of original papers and reviews based on results from molecular viewpoints.

Prof. Dr. Naoko Kanda
Guest Editor

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Keywords

psoriasis
pathogenesis
therapy
genetic
epigenetic
biologics
comorbidity
arthritis

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Published Papers (5 papers)

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Research

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21 pages, 14664 KiB

Open AccessArticle

Dietary Fiber Inulin Improves Murine Imiquimod-Induced Psoriasis-like Dermatitis

by Mai Yoshida, Yoko Funasaka, Hidehisa Saeki, Masami Yamamoto and Naoko Kanda

Int. J. Mol. Sci. 2023, 24(18), 14197; https://doi.org/10.3390/ijms241814197 - 17 Sep 2023

Cited by 4 | Viewed by 2439

Abstract

Psoriasis is a chronic skin disease with interleukin (IL)-17-dominated inflammation and hyperproliferation of epidermis. Dietary fiber is fermented by the gut microbiome into short-chain fatty acids (SCFAs) that manifest anti-inflammatory effects. We examined if feeding with an inulin-enriched high-fiber diet (HFD) might improve topical imiquimod-induced psoriasis-like dermatitis in mice. HFD reduced thickening and total severity scores of imiquimod-induced dermatitis and reduced epidermal thickness, inflammatory infiltrates, including Ly6G+ neutrophils, and epidermal Ki67+ proliferating cells. HFD reduced mRNA levels of IL-17A, IL-17F, IL-22, IL-1β, tumor necrosis factor (TNF)-α, CXCL1, CXCL2, and keratin 16 and increased those of transforming growth factor (TGF)-β1 and cyclin-dependent kinase inhibitor 1A in imiquimod-induced dermatitis. In 16S rRNA sequencing of the gut microbiome, imiquimod increased relative abundance of phylum Firmicutes, while HFD increased that of phylum Bacteroidota and genus Bacteroides. HFD increased serum and fecal concentrations of SCFA propionate. Oral propionate reduced inflammatory infiltrates and epidermal Ki67+ cells and reduced mRNA levels of IL-17A, IL-17F, IL-17C, IL-22, IL-1β, IL-6, TNF-α, CXCL1, CCL20 and increased those of TGF-β1and IL-10 in imiquimod-indued dermatitis. Dietary inulin supplementation improves imiquimod-induced psoriasis-like dermatitis partially via propionate, and may be a promising adjunctive therapy for psoriasis. Full article

(This article belongs to the Special Issue Progress in the Pathogenesis and Therapeutics of Psoriasis)

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16 pages, 1622 KiB

Open AccessArticle

Cytokine Signatures in Psoriatic Arthritis Patients Indicate Different Phenotypic Traits Comparing Responders and Non-Responders of IL-17A and TNFα Inhibitors

by Marie Skougaard, Sisse Bolm Ditlev, Magnus Friis Søndergaard and Lars Erik Kristensen

Int. J. Mol. Sci. 2023, 24(7), 6343; https://doi.org/10.3390/ijms24076343 - 28 Mar 2023

Cited by 3 | Viewed by 2157

Abstract

This study aimed to explore the dynamic interactions between 32 cytokines and biomarkers in Psoriatic Arthritis (PsA) patients to compare cytokine signatures of treatment responders and non-responders. Biomarkers were measured before and after four months of treatment in 39 PsA patients initiating either Tumor Necrosis Factor alpha inhibitor (TNFi) or Interleukin-17A inhibitor (IL-17Ai). Response to treatment was defined by the composite measure, Disease Activity in Psoriatic Arthritis (DAPSA). A two-component principal component analysis (PCA) was implemented to describe cytokine signatures comparing DAPSA50 responders and non-responders. The cytokine signature of TNFi responders was driven by the correlated cytokines interferon γ (IFNγ) and IL-6, additionally associated with IL-12/IL-23p40, TNFα, and CRP, while the cytokine signature of TNFi non-responders was driven by the correlated cytokines IL-15, IL-8, and IFNγ. IL-17Ai responders were characterized by contributions of strongly correlated Th17 inflammatory cytokines, IL-17A, IL-12/IL-23p40, IL-22 to the cytokine signature, whereas IL-17A and IL-12/IL-23p40 did not demonstrate significant contribution in IL-17Ai non-responders. Based on PCA results it was possible to differentiate DAPSA50 responders and non-responders to treatment, endorsing additional examination of cytokine interaction models in PsA patients and supporting further PsA patient immune stratification to improve individualized treatment of PsA patients. Full article

(This article belongs to the Special Issue Progress in the Pathogenesis and Therapeutics of Psoriasis)

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21 pages, 12901 KiB

Open AccessArticle

Anti-Psoriatic Effect of Rheum palmatum L. and Its Underlying Molecular Mechanisms

by Ly Thi Huong Nguyen, Sang-Hyun Ahn, Heung-Mook Shin and In-Jun Yang

Int. J. Mol. Sci. 2022, 23(24), 16000; https://doi.org/10.3390/ijms232416000 - 15 Dec 2022

Cited by 10 | Viewed by 2644

Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disorder. Rheum palmatum L. is a common traditional medicinal herb with anti-inflammatory and immunomodulatory activities. This study aimed to investigate the anti-psoriatic effects of the ethanolic extract from R. palmatum L. (RPE) and its chemical constituents, as well as the mechanisms underlying their therapeutic significance. An imiquimod (IMQ)-induced psoriasis-like mouse model was used to examine the anti-psoriatic effect of RPE in vivo. Network pharmacological analysis was performed to investigate the potential targets and related pathways of the RPE components, including rhein, emodin, chrysophanol, aloe-emodin, and physcion. The anti-inflammatory effects and underlying mechanisms of these components were examined using in vitro models. Topical application of RPE alleviated psoriasis-like symptoms and reduced levels of inflammatory cytokines and proliferation markers in the skin. Network pharmacological analysis revealed that RPE components target 20 genes that are linked to psoriasis-related pathways, such as IL-17, MAPK, and TNF signaling pathways. Among the five components of RPE, rhein and emodin showed inhibitory effects on TNF-α and IL-17 production in EL-4 cells, attenuated the production of CXCL8, CXCL10, CCL20, and MMP9, and reduced proliferation in HaCaT cells. Chrysophanol, aloe-emodin, and physcion were less effective than rhein and emodin in suppressing inflammatory responses and keratinocyte proliferation. The effects of these compounds might occur through the inhibition of the ERK, STAT3, and NF-κB signaling pathways. This study suggested the anti-psoriatic effect of RPE, with rhein and emodin as the main contributors that regulate multiple signaling pathways. Full article

(This article belongs to the Special Issue Progress in the Pathogenesis and Therapeutics of Psoriasis)

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Review

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17 pages, 1126 KiB

Open AccessReview

A Route for Investigating Psoriasis: From the Perspective of the Pathological Mechanisms and Therapeutic Strategies of Cancer

by Xingkang Wu, Yushuang Ma, Lu Wang and Xuemei Qin

Int. J. Mol. Sci. 2023, 24(18), 14390; https://doi.org/10.3390/ijms241814390 - 21 Sep 2023

Cited by 5 | Viewed by 2258

Abstract

Psoriasis is an incurable skin disease that develops in about two-thirds of patients before the age of 40 and requires lifelong treatment; its pathological mechanisms have not been fully elucidated. The core pathological process of psoriasis is epidermal thickening caused by the excessive proliferation of epidermal keratinocytes, which is similar to the key feature of cancer; the malignant proliferation of cancer cells causes tumor enlargement, suggesting that there is a certain degree of commonality between psoriasis and cancer. This article reviews the pathological mechanisms that are common to psoriasis and cancer, including the interaction between cell proliferation and an abnormal immune microenvironment, metabolic reprogramming, and epigenetic reprogramming. In addition, there are common therapeutic agents and drug targets between psoriasis and cancer. Thus, psoriasis and cancer share a common pathological mechanisms–drug targets–therapeutic agents framework. On this basis, it is proposed that investigating psoriasis from a cancer perspective is beneficial to enriching the research strategies related to psoriasis. Full article

(This article belongs to the Special Issue Progress in the Pathogenesis and Therapeutics of Psoriasis)

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24 pages, 1523 KiB

Open AccessReview

The Role of Adipokines in the Pathogenesis of Psoriasis

by Kajetan Kiełbowski, Estera Bakinowska, Piotr Ostrowski, Bartłomiej Pala, Ewa Gromowska, Klaudia Gurazda, Paweł Dec, Andrzej Modrzejewski and Andrzej Pawlik

Int. J. Mol. Sci. 2023, 24(7), 6390; https://doi.org/10.3390/ijms24076390 - 28 Mar 2023

Cited by 19 | Viewed by 3190

Abstract

Psoriasis is a chronic and immune-mediated skin condition characterized by pro-inflammatory cytokines and keratinocyte hyperproliferation. Dendritic cells, T lymphocytes, and keratinocytes represent the main cell subtypes involved in the pathogenesis of psoriasis, while the interleukin-23 (IL-23)/IL-17 pathway enhances the disease progression. Human adipose tissue is an endocrine organ, which secretes multiple proteins, known as adipokines, such as adiponectin, leptin, visfatin, or resistin. Current evidence highlights the immunomodulatory roles of adipokines, which may contribute to the progression or suppression of psoriasis. A better understanding of the complexity of psoriasis pathophysiology linked with adipokines could result in developing novel diagnostic or therapeutic strategies. This review aims to present the pathogenesis of psoriasis and the roles of adipokines in this process. Full article

(This article belongs to the Special Issue Progress in the Pathogenesis and Therapeutics of Psoriasis)

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