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Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0
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Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 11575

Special Issue Editor

Dr. Sandrine Dubrac

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Guest Editor
Department of Dermatology, Venereology and Allergology, Medical University of Innsbruck, 6020 Innsbruck, Austria
Interests: lipids; xenobiotic metabolism; PPAR; PXR mitochondria; peroxisomes; skin immunology; langerhans cells; atopic dermatitis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Atopic dermatitis and psoriasis are two devastating, chronic and pruritic inflammatory skin diseases with high prevalence worldwide. Atopic dermatitis and psoriasis have pathophysiological commonalities, including an impaired epidermal barrier, immune hyper-responsiveness, and local and systemic symptoms modulated by environmental factors, such as the skin microbiota and stress. Moreover, they both have a strong genetic component. In the past few years, tremendous effort has been invested into research to make progress in understanding their underlying pathomechanisms. However, owing to their etiological complexity combined with the identification of several disease endotypes, we still do not understand how and why these diseases develop.

The latest research has allowed us to decipher in detail several important aspects of the cellular and molecular abnormities involved in atopic dermatitis and psoriasis pathogenesis, and it has enabled the development of specific therapeutic strategies, namely, biologics. However, other therapeutic options might emerge from novel research, going beyond the current paradigms.

This Special Issue of IJMS welcomes a broad range of basic, preclinical and translational original and review articles focused on groundbreaking research in the fields of both atopic dermatitis and psoriasis.

Dr. Sandrine Dubrac
Guest Editor

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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.

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Published Papers (5 papers)

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Research

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13 pages, 2488 KiB  
Article
Stress Affects Mast Cell Proteases in Murine Skin in a Model of Atopic Dermatitis-like Allergic Inflammation
by Frank R. Rommel, Susanne Tumala, Anna-Lena Urban, Frank Siebenhaar, Johannes Kruse, Uwe Gieler and Eva M. J. Peters
Int. J. Mol. Sci. 2024, 25(11), 5738; https://doi.org/10.3390/ijms25115738 - 24 May 2024
Viewed by 224
Abstract
Stress exposure worsens allergic inflammatory diseases substantially. Mast cells (MCs) play a key role in peripheral immune responses to neuroendocrine stress mediators such as nerve growth factor (NGF) and substance P (SP). Mast cell proteases (MCPs) and cholinergic factors (Chrna7, SLURP1) were recently [...] Read more.
Stress exposure worsens allergic inflammatory diseases substantially. Mast cells (MCs) play a key role in peripheral immune responses to neuroendocrine stress mediators such as nerve growth factor (NGF) and substance P (SP). Mast cell proteases (MCPs) and cholinergic factors (Chrna7, SLURP1) were recently described to modulate MC stress response. We studied MCPs and Chrna7/SLURP1 and their interplay in a mouse model for noise induced stress (NiS) and atopic dermatitis-like allergic inflammation (AlD) and in cultured MC lacking Chrna7. We found that the cholinergic stress axis interacts with neuroendocrine stress mediators and stress-mediator cleaving enzymes in AlD. SP-cleaving mMCP4+ MC were upregulated in AlD and further upregulated by stress in NiS+AlD. Anti-NGF neutralizing antibody treatment blocked the stress-induced upregulation in vivo, and mMCP4+ MCs correlated with measures of AlD disease activity. Finally, high mMCP4 production in response to SP depended on Chrna7/SLURP1 in cultured MCs. In conclusion, mMCP4 and its upstream regulation by Chrna7/SLURP1 are interesting novel targets for the treatment of allergic inflammation and its aggravation by stress. Full article
(This article belongs to the Special Issue Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0)
23 pages, 5268 KiB  
Article
A Novel E3 Probiotics Formula Restored Gut Dysbiosis and Remodelled Gut Microbial Network and Microbiome Dysbiosis Index (MDI) in Southern Chinese Adult Psoriasis Patients
by Chi Tung Choy, Un Kei Chan, Pui Ling Kella Siu, Junwei Zhou, Chi Ho Wong, Yuk Wai Lee, Ho Wang Chan, Joseph Chi Ching Tsui, Steven King Fan Loo and Stephen Kwok Wing Tsui
Int. J. Mol. Sci. 2023, 24(7), 6571; https://doi.org/10.3390/ijms24076571 - 31 Mar 2023
Cited by 10 | Viewed by 4169
Abstract
Psoriasis is a common chronic immune-mediated inflammatory skin disease with the association of various comorbidities. Despite the introduction of highly effective biologic therapies over the past few decades, the exact trigger for an immune reaction in psoriasis is unclear. With the majority of [...] Read more.
Psoriasis is a common chronic immune-mediated inflammatory skin disease with the association of various comorbidities. Despite the introduction of highly effective biologic therapies over the past few decades, the exact trigger for an immune reaction in psoriasis is unclear. With the majority of immune cells residing in the gut, the effect of gut microbiome dysbiosis goes beyond the gastrointestinal site and may exacerbate inflammation and regulate the immune system elsewhere, including but not limited to the skin via the gut-skin axis. In order to delineate the role of the gut microbiome in Southern Chinese psoriasis patients, we performed targeted 16S rRNA sequencing and comprehensive bioinformatic analysis to compare the gut microbiome profile of 58 psoriasis patients against 49 healthy local subjects presumably with similar lifestyles. Blautia wexlerae and Parabacteroides distasonis were found to be enriched in psoriasis patients and in some of the healthy subjects, respectively. Metabolic functional pathways were predicted to be differentially abundant, with a clear shift toward SCFA synthesis in healthy subjects. The alteration of the co-occurrence network was also evident in the psoriasis group. In addition, we also profiled the gut microbiome in 52 of the 58 recruited psoriasis patients after taking 8 weeks of an orally administrated novel E3 probiotics formula (with prebiotics, probiotics and postbiotics). The Dermatological Life Quality Index (p = 0.009) and Psoriasis Area and Severity Index (p < 0.001) were significantly improved after taking 8 weeks of probiotics with no adverse effect observed. We showed that probiotics could at least partly restore gut dysbiosis via the modulation of the gut microbiome. Here, we also report the potential application of a machine learning-derived gut dysbiosis index based on a quantitative PCR panel (AUC = 0.88) to monitor gut dysbiosis in psoriasis patients. To sum up, our study suggests the gut microbial landscape differed in psoriasis patients at the genera, species, functional and network levels. Additionally, the dysbiosis index could be a cost-effective and rapid tool to monitor probiotics use in psoriasis patients. Full article
(This article belongs to the Special Issue Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0)
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11 pages, 776 KiB  
Article
Impact of Obesity on the IL-6 Immune Marker and Th17 Immune Cells in C57BL/6 Mice Models with Imiquimod-Induced Psoriasis
by So Hee Park, Kyung Ah Lee, Jae-Hyeog Choi, SaeGwang Park, Dae-Wook Kim and So Young Jung
Int. J. Mol. Sci. 2023, 24(6), 5592; https://doi.org/10.3390/ijms24065592 - 15 Mar 2023
Cited by 4 | Viewed by 1973
Abstract
Obese psoriatic patients experience higher disease severity and exhibit poorer treatment responses and clinical outcomes. It has been proposed that proinflammatory cytokines produced by adipose tissue exacerbate psoriasis; however, the role of obesity in psoriasis remains unclear. This study aimed to elucidate the [...] Read more.
Obese psoriatic patients experience higher disease severity and exhibit poorer treatment responses and clinical outcomes. It has been proposed that proinflammatory cytokines produced by adipose tissue exacerbate psoriasis; however, the role of obesity in psoriasis remains unclear. This study aimed to elucidate the role of obesity in the pathogenesis of psoriasis, focusing on immunological changes. To induce obesity, mice were fed a high-fat diet for 20 weeks. We then applied imiquimod to the skin on a mouse’s back for seven consecutive days to induce psoriasis and scored lesion severity every day for seven days. Cytokine levels in serum and the Th17 cell population in the spleen and draining lymph nodes were studied to identify immunological differences. The clinical severity was more remarkable, and histologically the epidermis was also significantly thicker in the obese group. Increased levels of IL-6 and TNF-α were observed in serum after psoriasis. They were elevated to a greater degree, with greater expansion of the functional Th17 cell population in the obese group. It is concluded that obesity could exacerbate psoriasis through mechanisms that involve elevated proinflammatory cytokine secretion and an expanded Th17 cell population. Full article
(This article belongs to the Special Issue Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0)
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Review

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17 pages, 1940 KiB  
Review
Regulatory Mechanism of the IL-33–IL-37 Axis via Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis
by Gaku Tsuji, Kazuhiko Yamamura, Koji Kawamura, Makiko Kido-Nakahara, Takamichi Ito and Takeshi Nakahara
Int. J. Mol. Sci. 2023, 24(19), 14633; https://doi.org/10.3390/ijms241914633 - 27 Sep 2023
Cited by 2 | Viewed by 1636
Abstract
Interleukin (IL)-33 and IL-37 have been identified as novel cytokines involved in various inflammatory diseases. However, their specific roles remain largely unknown. Recent studies have shown that IL-33, which triggers inflammation, and IL-37, which suppresses it, cooperatively regulate the balance between inflammation and [...] Read more.
Interleukin (IL)-33 and IL-37 have been identified as novel cytokines involved in various inflammatory diseases. However, their specific roles remain largely unknown. Recent studies have shown that IL-33, which triggers inflammation, and IL-37, which suppresses it, cooperatively regulate the balance between inflammation and anti-inflammation. IL-33 and IL-37 are also deeply involved in the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis. Furthermore, a signaling pathway by which aryl hydrocarbon receptor (AHR), a receptor for dioxins, regulates the expression of IL-33 and IL-37 has been revealed. Here, we outline recent findings on the mechanisms regulating IL-33 and IL-37 expression in AD and psoriasis. IL-33 expression is partially dependent on mitogen-activated protein kinase (MAPK) activation, and IL-37 has a role in suppressing MAPK in human keratinocytes. Furthermore, IL-33 downregulates skin barrier function proteins including filaggrin and loricrin, thereby downregulating the expression of IL-37, which colocalizes with these proteins. This leads to an imbalance of the IL-33–IL-37 axis, involving increased IL-33 and decreased IL-37, which may be associated with the pathogenesis of AD and psoriasis. Therefore, AHR-mediated regulation of the IL-33–IL-37 axis may lead to new therapeutic strategies for the treatment of AD and psoriasis. Full article
(This article belongs to the Special Issue Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0)
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17 pages, 2390 KiB  
Review
How to Understand Personalized Medicine in Atopic Dermatitis Nowadays?
by Alicja Mesjasz, Karol Kołkowski, Andreas Wollenberg and Magdalena Trzeciak
Int. J. Mol. Sci. 2023, 24(8), 7557; https://doi.org/10.3390/ijms24087557 - 20 Apr 2023
Cited by 1 | Viewed by 2848
Abstract
Atopic dermatitis (AD) is a heterogeneous disease in terms of its phenotypical, barrier, and immunological presentation. Emerging therapies are undoubtedly contributing to a new chapter in the treatment of AD, bringing an excellent possibility of individualization, and thereby creating a tailored approach. The [...] Read more.
Atopic dermatitis (AD) is a heterogeneous disease in terms of its phenotypical, barrier, and immunological presentation. Emerging therapies are undoubtedly contributing to a new chapter in the treatment of AD, bringing an excellent possibility of individualization, and thereby creating a tailored approach. The two most promising substance groups are biological drugs (dupilumab, tralokinumab, lebrikizumab, nemolizumab) and Janus kinase inhibitors (JAKis) (baricitinib, upadacitinib, and abrocitinib). The vision that certain well-defined phenotypes and endotypes, as well as personal preferences, may guide the future treatment of AD is both tempting and appealing, but not yet reality. The accessibility of new drugs such as biologics and small molecules has opened up the discussion regarding personalized medicine, referring to the complex nature of AD as well as the experiences from clinical trials and real-world evidence. We have now reached the point of creating new strategies and AD treatment goals by increasing the amount of new information concerning the efficacy and safety of new drugs. This article has reviewed the novel treatment options for AD in the light of the heterogeneity of this disease and proposes a broader vision on the strategy of personalized treatment of AD. Full article
(This article belongs to the Special Issue Atopic Dermatitis and Psoriasis Pathogenesis: Going beyond Paradigms 2.0)
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