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Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated
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Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated

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 December 2020) | Viewed by 95778

Special Issue Editor

Prof. Dr. Naoko Kanda

E-Mail Website
Guest Editor
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 abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes. Psoriatic patients are associated with arthritis in 6%–42% of cases, and are frequently associated with cardiometabolic syndromes. The dominance of the TNF-a/IL-23/IL-17 cytokine axis plays a central role in the immunopathogenesis of psoriasis, and treatment targeting these cytokines has remarkably improved the symptoms. In psoriatic skin lesions, TNF-a produced by pathogenetic dermal dendritic cells activates the same cells in an autocrine manner, and induces them to produce IL-23, which promotes the expansion of IL-17-producing cells like Th17, gdT, or type 3 innate lymphoid cells. Several chromosomal loci and single-nucleotide polymorphisms with susceptibility to psoriasis have been identified (PSORS1 locus, IL-23R, and IL-12B genes, etc.), In genetically susceptible individuals, exposure to environmental triggers like infection or biomechanical stress initiates an inflammatory cascade, ultimately creating a sustained inflammation. Epigenetic modifications of DNA methylation or histone acetylation/methylation are associated with the development of psoriasis. In this Special Issue, we will publish updated information regarding pathogenesis, comorbidities, and therapy of psoriasis. We warmly welcome your submissions of original papers and reviews based on results at the molecular level.

Prof. Naoko Kanda
Guest Editor

Manuscript Submission Information

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Keywords

  • IL-17
  • TNF-α
  • IL-23
  • biologic
  • arthritis
  • metabolic syndrome
  • T cell
  • dendritic cell
  • epigenetics

Published Papers (15 papers)

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Editorial

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5 pages, 194 KiB  
Editorial
Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated
by Naoko Kanda
Int. J. Mol. Sci. 2021, 22(6), 2979; https://doi.org/10.3390/ijms22062979 - 15 Mar 2021
Cited by 28 | Viewed by 5923
Abstract
Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. [...] Read more.
Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14/CARMA2sh. The blood cells of psoriasis patients showed the enhanced oxidative stress/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as Staphylococcus aureus and Streptococcus danieliae, which worsen the skin inflammation in turn. The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor γt inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)

Research

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10 pages, 3151 KiB  
Article
UBAC1/KPC2 Regulates TLR3 Signaling in Human Keratinocytes through Functional Interaction with the CARD14/CARMA2sh-TANK Complex
by Pellegrino Mazzone, Michele Congestrì, Ivan Scudiero, Immacolata Polvere, Serena Voccola, Lucrezia Zerillo, Gianluca Telesio, Pasquale Vito, Romania Stilo and Tiziana Zotti
Int. J. Mol. Sci. 2020, 21(24), 9365; https://doi.org/10.3390/ijms21249365 - 9 Dec 2020
Cited by 7 | Viewed by 2587
Abstract
CARD14/CARMA2 is a scaffold molecule whose genetic alterations are linked to human inherited inflammatory skin disorders. However, the mechanisms through which CARD14/CARMA2 controls innate immune response and chronic inflammation are not well understood. By means of a yeast two-hybrid screening, we identified the [...] Read more.
CARD14/CARMA2 is a scaffold molecule whose genetic alterations are linked to human inherited inflammatory skin disorders. However, the mechanisms through which CARD14/CARMA2 controls innate immune response and chronic inflammation are not well understood. By means of a yeast two-hybrid screening, we identified the UBA Domain Containing 1 (UBAC1), the non-catalytic subunit of the E3 ubiquitin-protein ligase KPC complex, as an interactor of CARMA2sh, the CARD14/CARMA2 isoform mainly expressed in human keratinocytes. UBAC1 participates in the CARMA2sh/TANK complex and promotes K63-linked ubiquitination of TANK. In human keratinocytes, UBAC1 negatively regulates the NF-κF-activating capacity of CARMA2sh following exposure to poly (I:C), an agonist of Toll-like Receptor 3. Overall, our data indicate that UBAC1 participates in the inflammatory signal transduction pathways involving CARMA2sh. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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15 pages, 1991 KiB  
Article
Reduced Proteasome Activity and Enhanced Autophagy in Blood Cells of Psoriatic Patients
by Piotr Karabowicz, Adam Wroński, Halina Ostrowska, Georg Waeg, Neven Zarkovic and Elżbieta Skrzydlewska
Int. J. Mol. Sci. 2020, 21(20), 7608; https://doi.org/10.3390/ijms21207608 - 14 Oct 2020
Cited by 12 | Viewed by 2562
Abstract
Psoriasis is a skin disease that is accompanied by oxidative stress resulting in modification of cell components, including proteins. Therefore, we investigated the relationship between the intensity of oxidative stress and the expression and activity of the proteasomal system as well as autophagy, [...] Read more.
Psoriasis is a skin disease that is accompanied by oxidative stress resulting in modification of cell components, including proteins. Therefore, we investigated the relationship between the intensity of oxidative stress and the expression and activity of the proteasomal system as well as autophagy, responsible for the degradation of oxidatively modified proteins in the blood cells of patients with psoriasis. Our results showed that the caspase-like, trypsin-like, and chymotrypsin-like activity of the 20S proteasome in lymphocytes, erythrocytes, and granulocytes was lower, while the expression of constitutive proteasome and immunoproteasome subunits in lymphocytes was increased cells of psoriatic patients compared to healthy subjects. Conversely, the expression of constitutive subunits in erythrocytes, and both constitutive and immunoproteasomal subunits in granulocytes were reduced. However, a significant increase in the autophagy flux (assessed using LC3BII/LC3BI ratio) independent of the AKT pathway was observed. The levels of 4-HNE, 4-HNE-protein adducts, and proteins carbonyl groups were significantly higher in the blood cells of psoriatic patients. The decreased activity of the 20S proteasome together with the increased autophagy and the significantly increased level of proteins carbonyl groups and 4-HNE-protein adducts indicate a proteostatic imbalance in the blood cells of patients with psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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13 pages, 865 KiB  
Article
Metabolic Syndrome, Clusterin and Elafin in Patients with Psoriasis Vulgaris
by Drahomira Holmannova, Pavel Borsky, Lenka Borska, Ctirad Andrys, Kvetoslava Hamakova, Vit Rehacek, Tereza Svadlakova, Andrea Malkova, Martin Beranek, Vladimir Palicka, Jan Krejsek and Zdenek Fiala
Int. J. Mol. Sci. 2020, 21(16), 5617; https://doi.org/10.3390/ijms21165617 - 5 Aug 2020
Cited by 13 | Viewed by 2814
Abstract
Background: Psoriasis is a pathological condition characterized by immune system dysfunction and inflammation. Patients with psoriasis are more likely to develop a wide range of disorders associated with inflammation. Serum levels of various substances and their combinations have been associated with the presence [...] Read more.
Background: Psoriasis is a pathological condition characterized by immune system dysfunction and inflammation. Patients with psoriasis are more likely to develop a wide range of disorders associated with inflammation. Serum levels of various substances and their combinations have been associated with the presence of the disease (psoriasis) and have shown the potential to reflect its activity. The aim of the present study is to contribute to the elucidation of pathophysiological links between psoriasis, its pro-inflammatory comorbidity metabolic syndrome (MetS), and the expression of clusterin and elafin, which are reflected in the pathophysiological “portfolio” of both diseases. Material and methods: Clinical examinations (PASI score), ELISA (clusterin, elafin), and biochemical analyses (parameters of MetS) were performed. Results: We found that patients with psoriasis were more often afflicted by MetS, compared to the healthy controls. Clusterin and elafin levels were higher in the patients than in the controls but did not correlate to the severity of psoriasis. Conclusion: Our data suggest that patients with psoriasis are more susceptible to developing other systemic inflammatory diseases, such as MetS. The levels of clusterin and elafin, which are tightly linked to inflammation, were significantly increased in the patients, compared to the controls, but the presence of MetS in patients did not further increase these levels. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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12 pages, 3316 KiB  
Article
Indoleamine 2,3-Dioxygenase 2 Deficiency Exacerbates Imiquimod-Induced Psoriasis-Like Skin Inflammation
by Kento Fujii, Yasuko Yamamoto, Yoko Mizutani, Kuniaki Saito and Mariko Seishima
Int. J. Mol. Sci. 2020, 21(15), 5515; https://doi.org/10.3390/ijms21155515 - 1 Aug 2020
Cited by 15 | Viewed by 3935
Abstract
Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme known to suppress immune responses, and several reports have showed that it is associated with psoriasis. IDO2 is an isoform of IDO1, recently identified as a catalytic enzyme in the tryptophan-kynurenine pathway, which [...] Read more.
Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme known to suppress immune responses, and several reports have showed that it is associated with psoriasis. IDO2 is an isoform of IDO1, recently identified as a catalytic enzyme in the tryptophan-kynurenine pathway, which is expressed in dendritic cells and monocytes. The expression of IDO2 in immune cells suggests that IDO2 may contribute to immune functions. However, the role of IDO2 in the pathogenesis of psoriasis remains unclear. In this study, to elucidate the role of IDO2 in psoriasis, we assessed imiquimod (IMQ)-induced psoriasis-like dermatitis in IDO2 knockout (KO) mice. Skin inflammation, evaluated by scoring erythema, scaling, and ear thickness, was significantly worse in the IDO2 KO mice than in the wild-type (WT) mice. The mRNA expression levels of TNF-α, IL-23p19, and IL-17A, key cytokines involved in the development of psoriasis, were also increased in the IDO2 KO mice. Furthermore, immunohistochemistry revealed that the number of Ki67-positive cells in the epidermis and CD4-, CD8-, and IL-17-positive lymphocytes infiltrating the dermis were significantly increased in the IDO2 KO mice. These results suggest that IDO2 might decrease IL-17 expression, thereby resulting in the suppression of skin inflammation in IMQ-induced psoriasis-like dermatitis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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17 pages, 3272 KiB  
Article
Changes in Proteome of Fibroblasts Isolated from Psoriatic Skin Lesions
by Agnieszka Gęgotek, Pedro Domingues, Adam Wroński and Elżbieta Skrzydlewska
Int. J. Mol. Sci. 2020, 21(15), 5363; https://doi.org/10.3390/ijms21155363 - 28 Jul 2020
Cited by 30 | Viewed by 2990
Abstract
The dermal fibroblasts are in constant contact with the cells of the immune system and skin epidermis. Therefore, they are essential for the development of lesions in psoriasis. The aim of this study was to assess the changes in the proteomic profile of [...] Read more.
The dermal fibroblasts are in constant contact with the cells of the immune system and skin epidermis. Therefore, they are essential for the development of lesions in psoriasis. The aim of this study was to assess the changes in the proteomic profile of fibroblasts in the dermis of psoriasis patients, and to discuss the most significant changes and their potential consequences. The proteomic results indicate that fibroblast dysfunction arises from the upregulation of proinflammatory factors and antioxidant proteins, as well as those involved in signal transduction and participating in proteolytic processes. Moreover, downregulated proteins in psoriatic fibroblasts are mainly responsible for the transcription/translation processes, glycolysis/ adenosine triphosphate synthesis and structural molecules. These changes can directly affect intercellular signaling and promote the hyperproliferation of epidermal cells. A better understanding of the metabolic effects of the proteomic changes observed could guide the development of new pharmacotherapies for psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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15 pages, 1451 KiB  
Article
Higher Serum Selenoprotein P Level as a Novel Inductor of Metabolic Complications in Psoriasis
by Anna Baran, Julia Nowowiejska, Julita Anna Krahel, Tomasz W. Kaminski, Magdalena Maciaszek and Iwona Flisiak
Int. J. Mol. Sci. 2020, 21(13), 4594; https://doi.org/10.3390/ijms21134594 - 28 Jun 2020
Cited by 12 | Viewed by 2568
Abstract
Selenoprotein P (SeP), a member of hepatokines, is involved in the development of various metabolic diseases closely related to psoriasis, but it has not been explored in that dermatosis so far. The study aimed to evaluate the clinical value of serum SeP concentrations [...] Read more.
Selenoprotein P (SeP), a member of hepatokines, is involved in the development of various metabolic diseases closely related to psoriasis, but it has not been explored in that dermatosis so far. The study aimed to evaluate the clinical value of serum SeP concentrations in patients with psoriasis and its interplay between disease activity, metabolic or inflammatory parameters and systemic therapy. The study included thirty-three patients with flared plaque-type psoriasis and fifteen healthy volunteers. Blood samples were collected before and after three months of treatment with methotrexate or acitretin. Serum SeP levels were evaluated using the immune–enzymatic method. SeP concentration was significantly higher in patients with psoriasis than in the controls (p < 0.05). Further, in patients with severe psoriasis, SeP was significantly increased, compared with the healthy volunteers before treatment, and significantly decreased after (p < 0.05, p = 0.041, respectively). SeP positively correlated with C-reactive protein and platelets and negatively with red blood counts (p = 0.008, p = 0.013, p = 0.022, respectively). Therapy resulted in a significant decrease in SeP level. Selenoprotein P may be a novel indicator of inflammation and the metabolic complications development in psoriatics, especially with severe form or with concomitant obesity. Classic systemic therapy has a beneficial effect on reducing the risk of comorbidities by inhibiting SeP. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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11 pages, 2304 KiB  
Article
The Role of Gut Microbiome in Psoriasis: Oral Administration of Staphylococcus aureus and Streptococcus danieliae Exacerbates Skin Inflammation of Imiquimod-Induced Psoriasis-Like Dermatitis
by Karin Okada, Yoshiaki Matsushima, Kento Mizutani and Keiichi Yamanaka
Int. J. Mol. Sci. 2020, 21(9), 3303; https://doi.org/10.3390/ijms21093303 - 7 May 2020
Cited by 32 | Viewed by 5045
Abstract
Psoriasis is one of the common chronic inflammatory skin diseases in which inflammatory cytokines such as IL-17 and TNF-α play critical roles. Skin microbiome of psoriasis patients is reported to have elevated Staphylococcus and Streptococcus genus. There are controversial reports about gut microbiome [...] Read more.
Psoriasis is one of the common chronic inflammatory skin diseases in which inflammatory cytokines such as IL-17 and TNF-α play critical roles. Skin microbiome of psoriasis patients is reported to have elevated Staphylococcus and Streptococcus genus. There are controversial reports about gut microbiome of psoriasis patients, and whether the diversity of bacteria in genus level is decreased or not is still unclear. Moreover, it is not yet known if these gut bacteria would be the cause of the inflammation or the result of the inflammation. We analyzed the gut microbiome of the inflammatory skin model mouse (keratinocyte-specific caspase-1 transgenic (Kcasp1Tg) mouse), by analyzing the 16S rRNA gene. Staphylocuccus aureus and Streptococcus danieliae were abundant in Kcasp1Tg mouse fecal microbiome. These dominant bacteria as well as recessive control bacteria were orally administrated to antibiotic-treated wild type mice, and set up imiquimod-induced psoriasis-like skin inflammation model. The skin inflammation including ear thickness and histopathological findings was analyzed. The exacerbated skin lesions with the elevated levels of TNF-α, IL-17A, IL-17F, and IL-22 were observed in Staphylocuccus aureus and Streptococcus danieliae administrated groups. Our finding suggests that there is affinity between skin inflammation severity and certain gut bacteria leading to a vicious cycle: skin inflammation populates certain gut bacteria which itself worsens the skin inflammation. This is the first report on Staphylocuccus aureus and Streptococcuus danieliae effects in vivo. Not only treating the skin lesion but also treating the gut microbiome could be the future key treatment for inflammatory skin disease such as psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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Review

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26 pages, 1312 KiB  
Review
Molecular and Cellular Mechanisms of Itch in Psoriasis
by Eriko Komiya, Mitsutoshi Tominaga, Yayoi Kamata, Yasushi Suga and Kenji Takamori
Int. J. Mol. Sci. 2020, 21(21), 8406; https://doi.org/10.3390/ijms21218406 - 9 Nov 2020
Cited by 55 | Viewed by 8888
Abstract
Itch (or pruritus) was not previously recognized as a serious symptom of psoriasis. However, approximately 60–90% of psoriatic patients with pruritus have stated that it deteriorates their quality of life. Since conventional antipruritic therapies, such as antihistamines, only exert limited effects, the establishment [...] Read more.
Itch (or pruritus) was not previously recognized as a serious symptom of psoriasis. However, approximately 60–90% of psoriatic patients with pruritus have stated that it deteriorates their quality of life. Since conventional antipruritic therapies, such as antihistamines, only exert limited effects, the establishment of a treatment option for itch in psoriasis is urgently needed. Although a definitive drug is not currently available, various itch mediators are known to be involved in pruritus in psoriasis. In this review, we describe the clinical features of pruritus in psoriasis, classify a wide range of itch mediators into categories, such as the nervous, immune, endocrine, and vascular systems, and discuss the mechanisms by which these mediators induce or aggravate itch in the pathophysiology of psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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16 pages, 689 KiB  
Review
New Treatment Addressing the Pathogenesis of Psoriasis
by Michio Tokuyama and Tomotaka Mabuchi
Int. J. Mol. Sci. 2020, 21(20), 7488; https://doi.org/10.3390/ijms21207488 - 11 Oct 2020
Cited by 127 | Viewed by 14791
Abstract
Psoriasis is an immune cell-mediated inflammatory skin disease. The interleukin (IL)23/IL17 axis plays an important role in the development of psoriasis. The effectiveness of biologic treatments such as tumor necrosis factor (TNF)α inhibitors (infliximab, adalimumab, certolizumab pegol), IL23 inhibitors (ustekinumab, guselkumab, tildrakizumab, risankizumab), [...] Read more.
Psoriasis is an immune cell-mediated inflammatory skin disease. The interleukin (IL)23/IL17 axis plays an important role in the development of psoriasis. The effectiveness of biologic treatments such as tumor necrosis factor (TNF)α inhibitors (infliximab, adalimumab, certolizumab pegol), IL23 inhibitors (ustekinumab, guselkumab, tildrakizumab, risankizumab), and IL17 inhibitors (secukinumab, ixekizumab, brodalumab) have verified these findings. Immune-related cells such as dendritic cells (DCs) and macrophages, in addition to Toll-like receptors and cytokines such as interferon (IFN)α, TNFα, IFNɤ, IL12, IL22, IL23, and IL17, are related to the pathogenesis of psoriasis. Here, we first review new insights regarding the pathogenesis of psoriasis, as it relates to DCs, Langerhans cells, macrophages, the signal transducer and activator of transcription 3 pathway, and aryl hydrocarbon receptor in cutaneous vascular endothelial cells. Based on these findings, we summarize currently available oral treatments and biologics. Furthermore, we describe a new treatment option including Janus kinase inhibitor, tyrosine kinase 2 inhibitor, modulator of sphingosine 1-phosphate receptor 1, and Rho-associated kinase 2 inhibitor. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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17 pages, 1846 KiB  
Review
Psoriasis and Antimicrobial Peptides
by Toshiya Takahashi and Kenshi Yamasaki
Int. J. Mol. Sci. 2020, 21(18), 6791; https://doi.org/10.3390/ijms21186791 - 16 Sep 2020
Cited by 67 | Viewed by 9097
Abstract
Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these cells and activate the innate immune system through various [...] Read more.
Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these cells and activate the innate immune system through various mechanisms to induce inflammation, thus participating in the pathogenesis of psoriasis. In particular, these antimicrobial peptides enhance the binding of damage-associated molecular patterns such as self-DNA and self-RNA to their receptors and promote the secretion of interferon from activated plasmacytoid dendritic cells and keratinocytes to promote inflammation in psoriasis. Neutrophil extracellular traps (NETs), complexes of self-DNA and proteins including LL-37 released from neutrophils in psoriatic skin, induce Th17. Activated myeloid dendritic cells secrete a mass of inflammatory cytokines such as IL-12 and IL-23 in psoriasis, which is indispensable for the proliferation and survival of T cells that produce IL-17. AMPs enhance the production of some of Th17 and Th1 cytokines and modulate receptors and cellular signaling in psoriasis. Inflammation induced by DAMPs, including self-DNA and RNA released due to microinjuries or scratches, and the enhanced recognition of DAMPs by AMPs, may be involved in the mechanism underlying the Köbner phenomenon in psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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17 pages, 2550 KiB  
Review
Role of Innate Immune Cells in Psoriasis
by Yuki Sato, Eisaku Ogawa and Ryuhei Okuyama
Int. J. Mol. Sci. 2020, 21(18), 6604; https://doi.org/10.3390/ijms21186604 - 9 Sep 2020
Cited by 43 | Viewed by 5570
Abstract
Psoriasis is a chronic inflammatory skin condition caused by a combination of hereditary and environmental factors. Its development is closely related to the adaptive immune response. T helper 17 cells are major IL-17-producing cells, a function that plays an important role in the [...] Read more.
Psoriasis is a chronic inflammatory skin condition caused by a combination of hereditary and environmental factors. Its development is closely related to the adaptive immune response. T helper 17 cells are major IL-17-producing cells, a function that plays an important role in the pathogenesis of psoriasis. However, recent findings have demonstrated that innate immune cells also contribute to the development of psoriasis. Innate lymphoid cells, γδ T cells, natural killer T cells, and natural killer cells are activated in psoriasis, contributing to disease pathology through IL-17-dependent and -independent mechanisms. The present review provides an overview of recent findings, demonstrating a role for innate immunity in psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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15 pages, 649 KiB  
Review
Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis
by Joanna Pleńkowska, Magdalena Gabig-Cimińska and Paweł Mozolewski
Int. J. Mol. Sci. 2020, 21(17), 6206; https://doi.org/10.3390/ijms21176206 - 27 Aug 2020
Cited by 80 | Viewed by 5687
Abstract
This review discusses how oxidative stress (OS), an imbalance between oxidants and antioxidants in favor of the oxidants, increased production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), and decreased concentration/activity of antioxidants affect the pathogenesis or cause the enhancement of psoriasis (Ps). [...] Read more.
This review discusses how oxidative stress (OS), an imbalance between oxidants and antioxidants in favor of the oxidants, increased production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), and decreased concentration/activity of antioxidants affect the pathogenesis or cause the enhancement of psoriasis (Ps). Here, we also consider how ROS/RNS-induced stress modulates the activity of transcriptional factors and regulates numerous protein kinase cascades that participate in the regulation of crosstalk between autophagy, apoptosis, and regeneration. Answers to these questions will likely uncover novel strategies for the treatment of Ps. Action in the field will avoid destructive effects of ROS/RNS-mediated OS resulting in cellular dysfunction and cell death. The combination of the fragmentary information on the role of OS can provide evidence to extend the full picture of Ps. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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14 pages, 1199 KiB  
Review
Psoriasis and Connective Tissue Diseases
by Toshiyuki Yamamoto
Int. J. Mol. Sci. 2020, 21(16), 5803; https://doi.org/10.3390/ijms21165803 - 13 Aug 2020
Cited by 12 | Viewed by 3922
Abstract
Psoriasis is a chronic systemic inflammatory disease with various co-morbidities, having been recently considered as a comprehensive disease named psoriatic disease or psoriatic syndrome. Autoimmune diseases are one form of its co-morbidities. In addition to the genetic background, shared pathogenesis including innate immunity, [...] Read more.
Psoriasis is a chronic systemic inflammatory disease with various co-morbidities, having been recently considered as a comprehensive disease named psoriatic disease or psoriatic syndrome. Autoimmune diseases are one form of its co-morbidities. In addition to the genetic background, shared pathogenesis including innate immunity, neutrophil extracellular trap (NETs), and type I interferon, as well as acquitted immunity such as T helper-17 (Th17) related cytokines are speculated to play a significant role in both psoriasis and connective tissue diseases. On the other hand, there are definite differences between psoriasis and connective tissue diseases, such as their pathomechanisms and response to drugs. Therefore, we cannot expect that one stone kills two birds, and thus caution is necessary when considering whether the administered drug for one disease is effective or not for another disease. In this review, several connective tissue diseases and related diseases are discussed from the viewpoint of their coexistence with psoriasis. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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19 pages, 816 KiB  
Review
Nutrition and Psoriasis
by Naoko Kanda, Toshihiko Hoashi and Hidehisa Saeki
Int. J. Mol. Sci. 2020, 21(15), 5405; https://doi.org/10.3390/ijms21155405 - 29 Jul 2020
Cited by 69 | Viewed by 18249
Abstract
Psoriasis is a chronic inflammatory skin disease characterized by accelerated tumor necrosis factor-α/interleukin-23/interleukin-17 axis, hyperproliferation and abnormal differentiation of epidermal keratinocytes. Psoriasis patients are frequently associated with obesity, diabetes, dyslipidemia, cardiovascular diseases, or inflammatory bowel diseases. Psoriasis patients often show unbalanced dietary habits [...] Read more.
Psoriasis is a chronic inflammatory skin disease characterized by accelerated tumor necrosis factor-α/interleukin-23/interleukin-17 axis, hyperproliferation and abnormal differentiation of epidermal keratinocytes. Psoriasis patients are frequently associated with obesity, diabetes, dyslipidemia, cardiovascular diseases, or inflammatory bowel diseases. Psoriasis patients often show unbalanced dietary habits such as higher intake of fat and lower intake of fish or dietary fibers, compared to controls. Such dietary habits might be related to the incidence and severity of psoriasis. Nutrition influences the development and progress of psoriasis and its comorbidities. Saturated fatty acids, simple sugars, red meat, or alcohol exacerbate psoriasis via the activation of nucleotide-binding domain, leucine-rich repeats containing family, pyrin domain-containing-3 inflammasome, tumor necrosis factor-α/interleukin-23/interleukin-17 pathway, reactive oxygen species, prostanoids/leukotrienes, gut dysbiosis or suppression of regulatory T cells, while n-3 polyunsaturated fatty acids, vitamin D, vitamin B12, short chain fatty acids, selenium, genistein, dietary fibers or probiotics ameliorate psoriasis via the suppression of inflammatory pathways above or induction of regulatory T cells. Psoriasis patients are associated with dysbiosis of gut microbiota and the deficiency of vitamin D or selenium. We herein present the update information regarding the stimulatory or regulatory effects of nutrients or food on psoriasis and the possible alleviation of psoriasis by nutritional strategies. Full article
(This article belongs to the Special Issue Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated)
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