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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 May 2022) | Viewed by 36516

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Special Issue Editors

Dr. Bogusław Nedoszytko

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Guest Editor

1. Department of Dermatology, Venereology and Allergology, Medical University of Gdansk, 80-214 Gdansk, Poland
2. Molecular Laboratory, Invicta Fertility and Reproductive Centre, 81-740 Sopot, Poland
Interests: genetic and epigenetic changes in mastocytosis; psoriasis; atopic dermatitis; treg regulation of skin immunology; chemokines and cytokines network in skin diseases; genetic and chromosomal changes in melanomas; sarcomas; T-cell lymphomas and breast carcinomas; genetic and chromosomal causes of infertility; preimplantation, prenatal and postnatal molecular and cytogenetic diagnostic
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Prof. Dr. Agnieszka Owczarczyk-Saczonek

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Guest Editor

Department of Dermatology, Sexually Transmitted Diseases and Clinical Immunology, School of Medicine, University of Warmia and Mazury in Olsztyn, 10-719 Olsztyn, Poland
Interests: psoriasis; inflammatory immune-mediated inflammatory disease; metabolic diseases
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Dorota Krasowska

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Guest Editor

Chair and Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, Lublin, Poland
Interests: psoriasis and comorbidities; atopic dermatitis; morphea; systemic sclerosis; skin cancers
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Dr. Aneta Szczerkowska-Dobosz

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Department of Dermatology, Venereology and Allergology, Medical University of Gdańsk, Gdańsk, Poland
Interests: psoriasis; psoriatic arthritis; granulomatous skin diseases; cutaneous complications of permanent pigmentation

Special Issue Information

Dear Colleagues,

Psoriasis is a common, chronic, inflammatory, immune-mediated skin disease affecting about 2% of the world's population. It is associated with many comorbidities including arthritis, metabolic syndrome and an increased cardiovascular disease risk, increasing the risk of mortality due to myocardial infarction and stroke.

The main cause of the disease is the overactivation of the skin's innate and acquired immune system cells by external factors (trauma, drugs and infections) and internal factors (stress, self DNA/AMP, and RNA/LL37). These cells secrete cytokines, chemokines and growth factors that stimulate keratinocyte proliferation, neoangiogenesis and inflammation. The IFNγ, TNFα and IL-23/IL17 axis, which activates the NF-κB pathway, plays a dominant role in the pathogenesis of the disease.

A complex interaction between epigenetics, genetics and the inflammatory signaling networks of skin and immune cell mediators has been proved in many studies.

Psoriasis has been shown to be associated with the mutation of more than 60 genes. They include genes encoding:

Cytokines and their receptors, which play a role in the formation and regulation of the function of Th17/Tc17, Th22, Th1, Th2 and NK cells.
Proteins related to the regulation of inflammatory processes related to the activation and regulation of the functions of pathways dependent on the transcription factor NF-κB.
Structural proteins of the epidermis.

Regarding epigenetic mechanisms, histone modifications, promoter methylations, and long noncoding RNA and microRNA hyperexpression are considered to be additional factors contributing to psoriasis pathogenesis, as they regulate abnormal keratinocyte differentiation and proliferation, aberrant keratinocyte–inflammatory cell communication, neoangiogenesis and chronic inflammation.

In this Special Issue, we will publish recent data regarding the pathogenesis, comorbidities and therapy of psoriasis. We invite you to submit original and review publications based on the results of molecular research.

Dr. Bogusław Nedoszytko
Prof. Dr. Agnieszka Owczarczyk-Saczonek
Prof. Dr. Dorota Krasowska
Dr. Aneta Szczerkowska-Dobosz
Guest Editors

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 submissions that pass pre-check are 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

psoriasis and psoriatic arthritis
IFNγ
TNFα
IL-23/IL-17 axis
genetic and epigenetic factors
metabolic risk factors
cardiometabolic syndromes
stress hormones
biologic therapy

Published Papers (10 papers)

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Editorial

Jump to: Research, Review

3 pages, 190 KiB

Open AccessEditorial

New Insights into Psoriasis

by Boguslaw Nedoszytko, Agnieszka Owczarczyk-Saczonek, Dorota Krasowska and Aneta Szczerkowska-Dobosz

Int. J. Mol. Sci. 2022, 23(21), 12851; https://doi.org/10.3390/ijms232112851 - 25 Oct 2022

Viewed by 986

Abstract

Psoriasis is a chronic inflammatory skin disease with many comorbidities resulting from not only local but also systemic inflammation [...] Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

Research

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16 pages, 2023 KiB

Open AccessArticle

Obesity and Dyslipidemia Synergistically Exacerbate Psoriatic Skin Inflammation

by Kenta Ikeda, Shin Morizane, Takahiko Akagi, Sumie Hiramatsu-Asano, Kota Tachibana, Ayano Yahagi, Masanori Iseki, Hideaki Kaneto, Jun Wada, Katsuhiko Ishihara, Yoshitaka Morita and Tomoyuki Mukai

Int. J. Mol. Sci. 2022, 23(8), 4312; https://doi.org/10.3390/ijms23084312 - 13 Apr 2022

Cited by 19 | Viewed by 3199

Abstract

Patients with psoriasis are frequently complicated with metabolic syndrome; however, it is not fully understood how obesity and dyslipidemia contribute to the pathogenesis of psoriasis. To investigate the mechanisms by which obesity and dyslipidemia exacerbate psoriasis using murine models and neonatal human epidermal keratinocytes (NHEKs), we used wild-type and Apoe-deficient dyslipidemic mice, and administered a high-fat diet for 10 weeks to induce obesity. Imiquimod was applied to the ear for 5 days to induce psoriatic dermatitis. To examine the innate immune responses of NHEKs, we cultured and stimulated NHEKs using IL-17A, TNF-α, palmitic acid, and leptin. We found that obesity and dyslipidemia synergistically aggravated psoriatic dermatitis associated with increased gene expression of pro-inflammatory cytokines and chemokines. Treatment of NHEKs with palmitic acid and leptin amplified pro-inflammatory responses in combination with TNF-α and IL-17A. Additionally, pretreatment with palmitic acid and leptin enhanced IL-17A-mediated c-Jun N-terminal kinase phosphorylation. These results revealed that obesity and dyslipidemia synergistically exacerbate psoriatic skin inflammation, and that metabolic-disorder-associated inflammatory factors, palmitic acid, and leptin augment the activation of epidermal keratinocytes. Our results emphasize that management of concomitant metabolic disorders is essential for preventing disease exacerbation in patients with psoriasis. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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17 pages, 2945 KiB

Open AccessArticle

The Effects of Vitamin D on the Expression of IL-33 and Its Receptor ST2 in Skin Cells; Potential Implication for Psoriasis

by Justyna M. Wierzbicka, Anna Piotrowska, Dorota Purzycka-Bohdan, Anna Olszewska, Joanna I. Nowak, Aneta Szczerkowska-Dobosz, Bogusław Nedoszytko, Roman J. Nowicki and Michał A. Żmijewski

Int. J. Mol. Sci. 2021, 22(23), 12907; https://doi.org/10.3390/ijms222312907 - 29 Nov 2021

Cited by 8 | Viewed by 2104

Abstract

Interleukin 33 (IL-33) belongs to the IL-1 family and is produced constitutively by epithelial and endothelial cells of various organs, such as the skin. It takes part in the maintenance of tissue homeostasis, repair, and immune response, including activation of Th2 lymphocytes. Its involvement in pathogenesis of several inflammatory diseases including psoriasis was also suggested, but this is not fully understood. The aim of the study was to investigate expression of IL-33 and its receptor, ST2, in psoriasis, and the effects of the active form of vitamin D (1,25(OH)₂D₃) on their expression in skin cells. Here we examined mRNA and protein profiles of IL-33 and ST2 in 18 psoriatic patients and healthy volunteers by qPCR and immunostaining techniques. Potential effects of 1,25(OH)₂D₃ and its receptor (VDR) on the expression of IL-33 and ST2 were tested in cultured keratinocytes, melanocytes, fibroblasts, and basal cell carcinoma cells. It was shown that 1,25(OH)₂D₃ effectively stimulated expression of IL-33 and its receptor ST2’s mRNAs in a time-dependent manner, in keratinocytes and to the lesser extends in melanocytes, but not in fibroblasts. Furthermore, the effect of vitamin D on expression of IL-33 and ST2 was VDR-dependent. Finally, we demonstrated that the expression of mRNA for IL-33 was mainly elevated in the psoriatic skin but not in its margin. Interestingly, ST2 mRNA was downregulated in psoriatic lesion compared to both marginal tissue as well as healthy skin. Our data indicated that vitamin D can modulate IL-33 signaling, opening up new perspectives for our understanding of the mechanism of vitamin D action in psoriasis therapy. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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19 pages, 3726 KiB

Open AccessArticle

Psoriasiform Inflammation Is Associated with Mitochondrial Fission/GDAP1L1 Signaling in Macrophages

by Ahmed Alalaiwe, Chi-Yuan Chen, Zi-Yu Chang, Jui-Tai Sung, Shih-Yi Chuang and Jia-You Fang

Int. J. Mol. Sci. 2021, 22(19), 10410; https://doi.org/10.3390/ijms221910410 - 27 Sep 2021

Cited by 11 | Viewed by 3004

Abstract

While psoriasis is known as a T cell- and dendritic cell-driven skin inflammation disease, macrophages are also reported to play some roles in its development. However, the signaling pathway of activated macrophages contributing to psoriasis is not entirely understood. Thus, we aimed to explore the possible mechanisms of how macrophages initiate and sustain psoriasis. The differentiated THP1 cells, stimulated by imiquimod (IMQ), were utilized as the activated macrophage model. IMQ was also employed to produce psoriasis-like lesions in mice. A transcriptomic assay of macrophages revealed that the expressions of pro-inflammatory mediators and GDAP1L1 were largely increased after an IMQ intervention. The depletion of GDAP1L1 by short hairpin (sh)RNA could inhibit cytokine release by macrophages. GDAP1L1 modulated cytokine production by activating the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB pathways. Besides GDAP1L1, another mitochondrial fission factor, Drp1, translocated from the cytosol to mitochondria after IMQ stimulation, followed by the mitochondrial fragmentation according to the immunofluorescence imaging. Clodronate liposomes were injected into the mice to deplete native macrophages for examining the latter’s capacity on IMQ-induced inflammation. The THP1 cells, with or without GDAP1L1 silencing, were then transplanted into the mice to monitor the deposition of macrophages. We found a significant THP1 accumulation in the skin and lymph nodes. The silencing of GDAP1L1 in IMQ-treated animals reduced the psoriasiform severity score from 8 to 2. After depleting GDAP1L1, the THP1 recruitment in the lymph nodes was decreased by 3-fold. The skin histology showed that the GDAP1L1-mediated macrophage activation induced neutrophil chemotaxis and keratinocyte hyperproliferation. Thus, mitochondrial fission can be a target for fighting against psoriatic inflammation. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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Review

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23 pages, 1598 KiB

Open AccessReview

Vitamin D Signaling in Psoriasis: Pathogenesis and Therapy

by Anna A. Brożyna, Radomir M. Slominski, Bogusław Nedoszytko, Michal A. Zmijewski and Andrzej T. Slominski

Int. J. Mol. Sci. 2022, 23(15), 8575; https://doi.org/10.3390/ijms23158575 - 02 Aug 2022

Cited by 17 | Viewed by 5291

Abstract

Psoriasis is a systemic, chronic, immune-mediated disease that affects approximately 2–3% of the world’s population. The etiology and pathophysiology of psoriasis are still unknown, but the activation of the adaptive immune system with the main role of T-cells is key in psoriasis pathogenesis. The modulation of the local neuroendocrine system with the downregulation of pro-inflammatory and the upregulation of anti-inflammatory messengers represent a promising adjuvant treatment in psoriasis therapies. Vitamin D receptors and vitamin D-mediated signaling pathways function in the skin and are essential in maintaining the skin homeostasis. The active forms of vitamin D act as powerful immunomodulators of clinical response in psoriatic patients and represent the effective and safe adjuvant treatments for psoriasis, even when high doses of vitamin D are administered. The phototherapy of psoriasis, especially UVB-based, changes the serum level of 25(OH)D, but the correlation of 25(OH)D changes and psoriasis improvement need more clinical trials, since contradictory data have been published. Vitamin D derivatives can improve the efficacy of psoriasis phototherapy without inducing adverse side effects. The anti-psoriatic treatment could include non-calcemic CYP11A1-derived vitamin D hydroxyderivatives that would act on the VDR or as inverse agonists on RORs or activate alternative nuclear receptors including AhR and LXRs. In conclusion, vitamin D signaling can play an important role in the natural history of psoriasis. Selective targeting of proper nuclear receptors could represent potential treatment options in psoriasis. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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21 pages, 1233 KiB

Open AccessReview

Killing Two Birds with One Stone: Potential Therapies Targeting Psoriasis and Atherosclerosis at the Same Time

by Eva Klara Merzel Šabović, Mateja Starbek Zorko and Miodrag Janić

Int. J. Mol. Sci. 2022, 23(12), 6648; https://doi.org/10.3390/ijms23126648 - 14 Jun 2022

Cited by 4 | Viewed by 2328

Abstract

Psoriasis is a chronic systemic inflammatory disease. Due to systemic inflammation, it is associated with many comorbidities. Among them, cardiovascular diseases represent the most common causes of morbidity and mortality in this population. Therefore, physicians treating patients with psoriasis should keep in mind that, as important as the treatment of psoriasis, awareness of cardiovascular risk deserves additional attention. Thus, in parallel with psoriasis treatment, a cardiovascular risk assessment must also be performed and addressed accordingly. In addition to encouraging non-pharmacologic strategies for a healthy lifestyle, physicians should be familiar with different pharmacologic options that can target psoriasis and reduce cardiovascular risk. In the present article, we present the pathophysiological mechanisms of the psoriasis and cardiometabolic interplay, our view on the interaction of psoriasis and cardiovascular disease, review the atherosclerotic effect of therapeutic options used in psoriasis, and vice versa, i.e., what the effect of medications used in the prevention of atherosclerosis could be on psoriasis. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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10 pages, 730 KiB

Open AccessReview

The Role of the Neutrophilic Network in the Pathogenesis of Psoriasis

by Joanna Czerwińska and Agnieszka Owczarczyk-Saczonek

Int. J. Mol. Sci. 2022, 23(3), 1840; https://doi.org/10.3390/ijms23031840 - 06 Feb 2022

Cited by 8 | Viewed by 2750

Abstract

One role of neutrophils, the most abundant innate immune sentinels, is neutrophil extracellular trap (NET) formation, which plays a significant role in immune surveillance. However, NET operation is bidirectional. Recent studies report that NETs may contribute to the development of autoimmune diseases such as psoriasis. The participation of neutrophils in the pathogenesis of that disease is dependent on an autoinflammatory feedback loop between neutrophils, lymphocytes, dendritic cells and keratinocytes. Our aim was to clarify the field of NET research in psoriasis and highlight the main factors required for NET generation, which may be a target of new therapies. This article presents a comphrehensive review concerning studies addressing the participation of neutrophils in the pathogenesis of psoriasis. Based on the available English-language literature, we discuss original papers presenting significant research findings which may help to understand and interpret the NET formation process in psoriasis, as well as the newest systematic reviews on PubMed. Next, the comparison, synthesis and summary of reported results were performed to clearly indicate the specific component of the NET which participates in the development of psoriasis. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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15 pages, 712 KiB

Open AccessReview

The Brain–Skin Axis in Psoriasis—Psychological, Psychiatric, Hormonal, and Dermatological Aspects

by Luiza Marek-Jozefowicz, Rafał Czajkowski, Alina Borkowska, Bogusław Nedoszytko, Michał A. Żmijewski, Wiesław J. Cubała and Andrzej T. Slominski

Int. J. Mol. Sci. 2022, 23(2), 669; https://doi.org/10.3390/ijms23020669 - 08 Jan 2022

Cited by 33 | Viewed by 8359

Abstract

Psoriasis is a chronic inflammatory skin disease with systemic manifestation, in which psychological factors play an important role. The etiology of psoriasis is complex and multifactorial, including genetic background and environmental factors such as emotional or physical stress. Psychological stress may also play a role in exacerbation of psoriasis, by dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, sympathetic–adrenal–medullary axis, peripheral nervous system, and immune system. Skin cells also express various neuropeptides and hormones in response to stress, including the fully functional analog of the HPA axis. The deterioration of psoriatic lesions is accompanied by increased production of inflammatory mediators, which could contribute to the imbalance of neurotransmitters and the development of symptoms of depression and anxiety. Therefore, deregulation of the crosstalk between endocrine, paracrine, and autocrine stress signaling pathways contributes to clinical manifestations of psoriasis, which requires multidisciplinary approaches. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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17 pages, 332 KiB

Open AccessReview

Analysis of the Potential Genetic Links between Psoriasis and Cardiovascular Risk Factors

by Dorota Purzycka-Bohdan, Anna Kisielnicka, Michał Bohdan, Aneta Szczerkowska-Dobosz, Marta Sobalska-Kwapis, Bogusław Nedoszytko and Roman J. Nowicki

Int. J. Mol. Sci. 2021, 22(16), 9063; https://doi.org/10.3390/ijms22169063 - 23 Aug 2021

Cited by 13 | Viewed by 3185

Abstract

Cardiovascular risk factors are one of the most common comorbidities in psoriasis. A higher prevalence of hypertension, insulin resistance and type 2 diabetes, dyslipidemia, obesity, metabolic syndrome, depression, as well as cardiovascular disease was confirmed in psoriatic patients in comparison to the general population. Data suggest that psoriasis and systemic inflammatory disorders may originate from the pleiotropic interactions with many genetic pathways. In this review, the authors present the current state of knowledge on the potential genetic links between psoriasis and cardiovascular risk factors. The understanding of the processes linking psoriasis with cardiovascular risk factors can lead to improvement of psoriasis management in the future. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

11 pages, 3390 KiB

Open AccessReview

Aberrations in Lipid Expression and Metabolism in Psoriasis

by Julia Nowowiejska, Anna Baran and Iwona Flisiak

Int. J. Mol. Sci. 2021, 22(12), 6561; https://doi.org/10.3390/ijms22126561 - 18 Jun 2021

Cited by 45 | Viewed by 3145

Abstract

Psoriasis (PSO) is a common skin disease that affects about 1%–3% of the general population. It is a great medical, social and economic burden since PSO is associated with many comorbidities, of which the most common are cardiometabolic disorders. Psoriatic patients suffer more frequently from obesity, dyslipidemia, atherosclerosis, and nonalcoholic fatty liver disease. Research shows that lipid expression and metabolism disorders are present more often in such patients. This review focuses on a variety of aberrations in lipids in the skin, blood, and adipose tissue in psoriatic patients and their multifactorial impact on the pathogenesis of psoriasis. Full article

(This article belongs to the Special Issue New Insights into Psoriasis)

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