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Recent Advances in Skin Disease and Comorbidities 2.0
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Recent Advances in Skin Disease and Comorbidities 2.0

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 (28 March 2024) | Viewed by 5266

Special Issue Editor

Prof. Dr. Yamanaka Keiichi

E-Mail Website
Guest Editor
Mie University Faculty of Medicine, Tsu, Japan
Interests: inflammatory skin disease; psoriasis; atopic dermatitis; cytokine; neutrophil
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The skin is one of the largest immune organs, involving both the innate and acquired immune systems. Skin is thus able to respond to exogenous stimuli, producing large quantities of proinflammatory cytokines and resulting in systemic inflammation.

In psoriasis, one of the intractable inflammatory cytokine-mediated skin disorders, the average life span is 6 years shorter compared to that of the population without a history of psoriasis; this difference is due to the cerebro-cardiovascular complications of the disease. Additionally, eczema patients are at an increased risk of cardiovascular disorders. Several studies have shown that severe inflammatory skin disorders are deeply connected to systemic complications, such as arteriosclerosis, cardiomyopathy, abnormal fat metabolism, nonalcoholic fatty liver disease, renal sclerosis, and systemic amyloidosis, leading to the concept of inflammatory skin march: intimate relationships between skin inflammation and complications.

For this new Special Issue, we welcome new advances and molecular research findings focusing on systemic inflammatory changes and systemic organ diseases complicated by inflammatory skin disorders. We warmly welcome the submission of both original papers and reviews.

Prof. Dr. Yamanaka Keiichi
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 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

  • inflammatory skin disease
  • psoriasis
  • atopic dermatitis
  • cytokine
  • comorbidity
  • complication
  • systemic inflammation
  • internal organs

Related Special Issue

Published Papers (4 papers)

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Research

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15 pages, 3460 KiB  
Article
Integrated Omics Analysis Uncovers the Culprit behind Exacerbated Atopic Dermatitis in a Diet-Induced Obesity Model
by You Mee Ahn, Jeeyoun Jung and So Min Lee
Int. J. Mol. Sci. 2024, 25(8), 4143; https://doi.org/10.3390/ijms25084143 - 9 Apr 2024
Viewed by 541
Abstract
Atopic dermatitis (AD), a chronic inflammatory skin disease, is exacerbated by obesity, yet the precise linking mechanism remains elusive. This study aimed to elucidate how obesity amplifies AD symptoms. We studied skin samples from three mouse groups: sham control, AD, and high-fat (HF) [...] Read more.
Atopic dermatitis (AD), a chronic inflammatory skin disease, is exacerbated by obesity, yet the precise linking mechanism remains elusive. This study aimed to elucidate how obesity amplifies AD symptoms. We studied skin samples from three mouse groups: sham control, AD, and high-fat (HF) + AD. The HF + AD mice exhibited more severe AD symptoms than the AD or sham control mice. Skin lipidome analysis revealed noteworthy changes in arachidonic acid (AA) metabolism, including increased expression of pla2g4, a key enzyme in AA generation. Genes for phospholipid transport (Scarb1) and acyltransferase utilizing AA as the acyl donor (Agpat3) were upregulated in HF + AD skin. Associations were observed between AA-containing phospholipids and skin lipids containing AA and its metabolites. Furthermore, imbalanced phospholipid metabolism was identified in the HF + AD mice, marked by excessive activation of the AA and phosphatidic acid (PA)-mediated pathway. This imbalance featured increased expression of Plcb1, Plcg1, and Dgk involved in PA generation, along with a decrease in genes converting PA into diglycerol (DG) and CDP-DG (Lpin1 and cds1). This investigation revealed imbalanced phospholipid metabolism in the skin of HF + AD mice, contributing to the heightened inflammatory response observed in HF + AD, shedding light on potential mechanisms linking obesity to the exacerbation of AD symptoms. Full article
(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities 2.0)
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16 pages, 8256 KiB  
Article
Increased Mortality Risk at Septic Condition in Inflammatory Skin Disorders and the Effect of High-Fat Diet Consumption
by Mai Nishimura, Takehisa Nakanishi, Masako Ichishi, Yoshiaki Matsushima, Masatoshi Watanabe and Keiichi Yamanaka
Int. J. Mol. Sci. 2024, 25(1), 478; https://doi.org/10.3390/ijms25010478 - 29 Dec 2023
Cited by 1 | Viewed by 909
Abstract
In recent years, attention has increasingly focused on various infectious diseases. Although some fatalities are directly attributed to the causative virus, many result from complications and reactive inflammation. Patients with comorbidities are at a higher risk of mortality. Refractory skin conditions such as [...] Read more.
In recent years, attention has increasingly focused on various infectious diseases. Although some fatalities are directly attributed to the causative virus, many result from complications and reactive inflammation. Patients with comorbidities are at a higher risk of mortality. Refractory skin conditions such as atopic dermatitis, psoriasis, and epidermolysis bullosa, known for an elevated risk of sepsis, partly owe this to compromised surface barrier function. However, the detailed mechanisms underlying this phenomenon remain elusive. Conversely, although the detrimental effects of a high-fat diet on health, including the onset of metabolic syndrome, are widely recognized, the association between diet and susceptibility to sepsis has not been extensively explored. In this study, we examined the potential causes and pathogenesis of increased sepsis susceptibility in inflammatory skin diseases using a mouse dermatitis model: keratin 14-driven caspase-1 is overexpressed (KCASP1Tg) in mice on a high-fat diet. Our findings reveal that heightened mortality in the dermatitis mouse model is caused by the inflamed immune system due to the chronic inflammatory state of the local skin, and administration of LPS causes a rapid increase in inflammatory cytokine levels in the spleen. Intake of a high-fat diet exacerbates these cytokine levels. Interestingly, we also observed a reduced expression of Toll-like receptor 4 (TLR4) in monocytes from KCASP1Tg mice, potentially predisposing these animals to heightened infection risks and associated complications. Histological analysis showed a clear decrease in T and B cells in the spleen of KCASP1Tg mice fed a high-fat diet. Thickening of the alveolar wall, inflammatory cell infiltration, and alveolar hemorrhage were more prominent in the lungs of KCASP1Tg and KCASP1Tg with fat mice. We postulate that the chronic, non-infectious inflammation induces a negative feedback loop within the inflammatory cascade, and the suppressed expression of TLR4 renders the mice more susceptible to infections. Therefore, it is imperative for individuals with chronic skin inflammation to closely monitor disease progression upon infection and seek timely and appropriate treatment. Additionally, chronic inflammation of adipose tissue, induced by high-fat food intake, combined with dermatitis inflammation, may exacerbate infections, necessitating a review of dietary habits. Full article
(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities 2.0)
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Review

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15 pages, 1013 KiB  
Review
Gastrointestinal Comorbidities Associated with Atopic Dermatitis—A Narrative Review
by Weronika Zysk, Alicja Mesjasz, Magdalena Trzeciak, Andrea Horvath and Katarzyna Plata-Nazar
Int. J. Mol. Sci. 2024, 25(2), 1194; https://doi.org/10.3390/ijms25021194 - 18 Jan 2024
Viewed by 1494
Abstract
The current understanding of atopic dermatitis (AD) seems to be extending beyond a skin-confined condition frequently associated with allergic comorbidities, as in a number of epidemiological studies, the prevalence rate of a range of illnesses has been determined to be greater in patients [...] Read more.
The current understanding of atopic dermatitis (AD) seems to be extending beyond a skin-confined condition frequently associated with allergic comorbidities, as in a number of epidemiological studies, the prevalence rate of a range of illnesses has been determined to be greater in patients with AD, or inversely. In most cases, the reasons for this are vague. A subset of these conditions are gastrointestinal disorders, including food sensitization (FS) and food allergy (FA), eosinophilic esophagitis (EoE) (it is of mixed background, both IgE-dependent and independent), food protein-induced enterocolitis syndrome (FPIES) (it exemplifies an IgE-independent food allergy), Crohn’s disease (CD), colitis ulcerosa (CU), celiac disease, irritable bowel syndrome (IBS), and gastroesophageal reflux disease (GERD). In this review, we performed a comprehensive search of the literature using the PubMed database. We addressed the epidemiology of the increased co-occurrence of these diseases with AD and discussed potential causes for this subject. Multiple gastroenterological comorbidities appear to be more common in patients with AD, according to our review. The mechanisms that underlie this phenomenon are largely unknown, highlighting the need for further study in this field. Full article
(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities 2.0)
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21 pages, 1041 KiB  
Review
Cytokines in Systemic Lupus Erythematosus—Focus on TNF-α and IL-17
by Patricia Richter, Luana Andreea Macovei, Ioana Ruxandra Mihai, Anca Cardoneanu, Maria Alexandra Burlui and Elena Rezus
Int. J. Mol. Sci. 2023, 24(19), 14413; https://doi.org/10.3390/ijms241914413 - 22 Sep 2023
Cited by 3 | Viewed by 1945
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder known for its complex pathogenesis, in which cytokines play an essential role. It seems that the modulation of these cytokines may impact disease progression, being considered potential biomarkers. Thus, TNF (tumor necrosis factor)-α and IL [...] Read more.
Systemic lupus erythematosus (SLE) is an autoimmune disorder known for its complex pathogenesis, in which cytokines play an essential role. It seems that the modulation of these cytokines may impact disease progression, being considered potential biomarkers. Thus, TNF (tumor necrosis factor)-α and IL (interleukin)-17 are molecules of great interest in SLE. TNF-α plays a dual role in SLE, with both immunosuppressive and proinflammatory functions. The role of IL-17 is clearly described in the pathogenesis of SLE, having a close association with IL-23 in stimulating the inflammatory response and consecutive tissue destruction. It appears that patients with elevated levels of these cytokines are associated with high disease activity expressed by the SLE disease activity index (SLEDAI) score, although some studies do not confirm this association. However, TNF-α and IL-17 are found in increased titers in lupus patients compared to the general population. Whether inhibition of these cytokines would lead to effective treatment is under discussion. In the case of anti-TNF-α therapies in SLE, the possibility of ATIL (anti-TNF-induced lupus) is a serious concern that limits their use. The use of anti-IL-17 therapies in SLE is a promising option, but not yet approved. Future studies of these cytokines in large cohorts will provide valuable information for the management of SLE. Full article
(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities 2.0)
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