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27 pages, 3429 KB

Open AccessArticle

The Dynamics of Blood-Count-Derived Inflammatory Indices in the Course of Systemic Treatment for Psoriasis: A Single Center Study

by Agnieszka Hołdrowicz, Daria Gierach-Michalska, Aleksandra Kośny, Radosław Zajdel and Agnieszka Żebrowska

Int. J. Mol. Sci. 2026, 27(3), 1612; https://doi.org/10.3390/ijms27031612 - 6 Feb 2026

Cited by 1 | Viewed by 991

Abstract

Psoriasis is a chronic inflammatory disease that affects up to 3% of the global population. In recent years, monoclonal antibodies targeting key cytokines underlying skin lesions and joint involvement in the course of psoriasis, i.e., TNF-α, IL-17, and IL-23, have been increasingly used [...] Read more.

Psoriasis is a chronic inflammatory disease that affects up to 3% of the global population. In recent years, monoclonal antibodies targeting key cytokines underlying skin lesions and joint involvement in the course of psoriasis, i.e., TNF-α, IL-17, and IL-23, have been increasingly used due to their high effectiveness and favorable safety profile. Numerous studies have been conducted analyzing the influence of cytokine inhibitors on non-specific inflammatory markers. However, only a limited number of studies on the effect of methotrexate (MTX) therapy on blood-count-derived inflammatory indices in patients with plaque psoriasis have been published so far. The study aims to analyze and compare the impact of methotrexate and biological drugs on the dynamics of selected blood-count-derived inflammatory indices in psoriatic patients. The analysis involved 182 patients receiving biological therapy, which resulted in a total of 219 treatment cycles (TCs) and 48 patients treated with therapeutic doses of MTX (48 TCs). In the biological subgroup, there were six TCs with an inhibitor of IL-12/23, 58 TCs with IL-17A inhibitors, 22 TCs with an inhibitor of IL-17AF, 113 TCs with IL-23 inhibitors, and 20 TCs with TNF-alfa inhibitors. A comparison between patients receiving biological treatment regardless of the drug and patients receiving MTX was conducted. Themajor factors determining the duration of MTX therapy were older age at the time of therapy initiation, a later onset of psoriasis, and a higher burden of comorbidities. Furthermore, the strongest impact on the average inflammatory state over time in patients treated with methotrexate was associated with comorbidities, male gender, and older age. Contrary to MTX therapy, patients receiving biological drugs were characterized by lower values of most assessed blood-count-derived inflammatory biomarkers at week 40 compared to baseline. It was confirmed that biologics and MTX treatment modify the dynamics of blood-count-derived inflammatory biomarkers in a different manner. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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12 pages, 2383 KB

Open AccessArticle

Mass Spectrometry Imaging Elucidates the Precise Localization and Site-Specific Functions of Skin Lipids

by Shown Tokoro, Tadayuki Ogawa, Shujiro Hayashi and Ken Igawa

Int. J. Mol. Sci. 2025, 26(24), 12114; https://doi.org/10.3390/ijms262412114 - 16 Dec 2025

Cited by 1 | Viewed by 971

Abstract

Lipids are essential for the skin, playing a crucial role in forming plasma membranes and maintaining the skin’s permeability barrier and hydration. Intercellular lipids fill the spaces between corneocytes and contribute to the barrier function. Lipid abnormalities in the skin have been observed [...] Read more.

Lipids are essential for the skin, playing a crucial role in forming plasma membranes and maintaining the skin’s permeability barrier and hydration. Intercellular lipids fill the spaces between corneocytes and contribute to the barrier function. Lipid abnormalities in the skin have been observed in many skin diseases, including atopic dermatitis and psoriasis. However, the specific localization and roles of skin lipids at particular sites remain incompletely elucidated due to the limited methods available for comprehensive lipid analysis. This study aims to precisely determine the localization of skin lipids, especially intercellular lipids, and investigate their roles and metabolism using mass spectrometry imaging (MSI). We conducted high-resolution (spatial resolution: 5 µm) matrix-assisted laser desorption/ionization (MALDI)-MSI on the lower back and buttocks and created overlay images of skin lipids to clarify their precise localizations. Ceramide was localized in the outermost layer among intercellular lipids. Cholesterol and free fatty acids were present in the stratum corneum but were at trace levels in the outermost layer. Cholesterol sulfate was abundant in the granular layer and gradually decreased in the stratum corneum, promoting desquamation. Phospholipids were confined to the viable epidermis (stratum corneum-/epidermis+), which forms the plasma membrane. A significant increase in mass intensity in the stratum corneum was observed for ceramide, sphingoid base, cholesterol, and free fatty acids, along with a decrease in phospholipids compared with those in the viable epidermis, based on region of interest analysis (Mann–Whitney test, p < 0.0005). We clarified the precise localization of skin lipids, particularly intercellular lipids. Our findings supported the reported functions of skin lipids at specific sites. Skin lipids are metabolized to form intercellular lipids in the stratum corneum, which are essential for the skin barrier. Our current lipid localization data serve as a baseline, or healthy control dataset, for future MSI-based lipid biomarker research in disease groups. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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11 pages, 1560 KB

Open AccessArticle

Serum Dysregulation of IL-36, IL-37, and IL-38 in Pyoderma Gangrenosum: Clinical Correlations and Implications for IL-36R-Targeted Therapy

by Magdalena Łyko, Joanna Maj, Klaudia Rubas, Anna Ryguła-Kowalska, Danuta Nowicka-Suszko and Alina Jankowska-Konsur

Int. J. Mol. Sci. 2025, 26(24), 12076; https://doi.org/10.3390/ijms262412076 - 15 Dec 2025

Viewed by 839

Abstract

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by chronic, painful ulcerations. Despite increasing evidence suggesting immunological dysregulation, the role of IL-36 cytokines in PG remains poorly defined. To evaluate serum levels of IL-36α, IL-36β, IL-36γ, IL-36Ra, IL-37, and IL-38 in PG [...] Read more.

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by chronic, painful ulcerations. Despite increasing evidence suggesting immunological dysregulation, the role of IL-36 cytokines in PG remains poorly defined. To evaluate serum levels of IL-36α, IL-36β, IL-36γ, IL-36Ra, IL-37, and IL-38 in PG patients compared to healthy controls, and to assess their correlation with selected clinical parameters and cytokine ratios. 44 PG patients and 40 healthy controls were included in this case–control study. Serum cytokine levels were measured using ELISA. Correlations between cytokine levels and clinical features were analyzed using nonparametric tests. PG patients showed significantly lower serum levels of IL-36α and IL-36γ (p = 0.0003 and p = 0.02, respectively), with no difference in IL-36β. Conversely, levels of IL-36Ra, IL-37, and IL-38 were significantly higher in PG patients (p < 0.0001 for all). In the PG group, significant positive correlations were observed between IL-36α and IL-36β, and between IL-36β and IL-36γ, while IL-37 correlated negatively with IL-38. IL-36α was inversely associated with serum IgA levels and total ulcer surface area, and IL-36γ correlated negatively with white blood cell count. Our findings reveal a dysregulated IL-36 cytokine profile in pyoderma gangrenosum, marked by reduced serum levels of IL-36α and IL-36γ and elevated levels of IL-36Ra, IL-37, and IL-38. This may reflect a compensatory response to chronic inflammation. The inverse correlation between IL-36α and ulcer size suggests its potential involvement in wound healing. Despite lower serum levels of agonists, local biological activity of IL-36 cytokines may remain elevated due to tissue-level activation and consumption. These results highlight the therapeutic relevance of targeting the IL-36 pathway—particularly in treatment-resistant cases—and support further research into cytokine activity beyond serum concentration to guide novel therapeutic strategies. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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17 pages, 5837 KB

Open AccessArticle

Therapeutic Effects of Sigesbeckia pubescens Makino Against Atopic Dermatitis-Like Skin Inflammation Through the JAK2/STAT Signaling Pathway

by Hyun-Kyung Song, Hye Jin Kim, Seong Cheol Kim and Taesoo Kim

Int. J. Mol. Sci. 2025, 26(9), 4191; https://doi.org/10.3390/ijms26094191 - 28 Apr 2025

Cited by 5 | Viewed by 1599

Abstract

Atopic dermatitis (AD), a chronic inflammatory skin condition, is a common allergic disorder. The human skin, the largest organ, serves as the first barrier in protecting the body against various external threats. Human epidermal keratinocytes (HEKs) in the epidermal layer and human dermal [...] Read more.

Atopic dermatitis (AD), a chronic inflammatory skin condition, is a common allergic disorder. The human skin, the largest organ, serves as the first barrier in protecting the body against various external threats. Human epidermal keratinocytes (HEKs) in the epidermal layer and human dermal fibroblasts (HDFs) in the dermis of the skin are implicated in AD-associated skin inflammation through the secretion of diverse inflammatory mediators, including chemokines. Sigesbeckia pubescens Makino (SP), a traditional Korean and Chinese herbal remedy, is used for treating inflammatory conditions. While several pharmacological effects of SP extract (SPE) have been documented, its specific inhibitory effect on AD-related skin inflammation remains unexplored. Hence, oral administration of SPE to NC/Nga mice reduced the severity of house dust mite extract-induced dermatitis, accompanied by lowered levels of serum inflammatory mediators, decreased epidermal thickness, reduced mast cell infiltration, and restoration of skin barrier function within skin lesions. In conclusion, SPE has demonstrated the ability to alleviate skin inflammation and protect the skin barrier and shows potential as a therapeutic option for AD. SPE inhibited proinflammatory chemokine production by modulating the Janus kinase (JAK) 2/signal transducer and activator of transcription proteins (STAT) 1/STAT3 signaling pathway in IFN-γ- and TNF-α-stimulated skin cells. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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18 pages, 3602 KB

Open AccessArticle

Peripheral Kynurenine Pathway Metabolites in Patients with Psoriasis

by Anna Stepaniuk, Anna Baran, Justyna Magdalena Hermanowicz, Beata Sieklucka, Dariusz Pawlak and Iwona Flisiak

Int. J. Mol. Sci. 2025, 26(7), 3139; https://doi.org/10.3390/ijms26073139 - 28 Mar 2025

Cited by 4 | Viewed by 1860

Abstract

Psoriasis is a systemic disease affecting 2–3% of the general population. Tryptophan (TRP) is an amino acid metabolized in the kynurenine pathway (KP). The aim of this study was to assess the kynurenine pathway’s metabolites in serum and urine of psoriatic patients and [...] Read more.

Psoriasis is a systemic disease affecting 2–3% of the general population. Tryptophan (TRP) is an amino acid metabolized in the kynurenine pathway (KP). The aim of this study was to assess the kynurenine pathway’s metabolites in serum and urine of psoriatic patients and explore the possible interplay with the disease’s pathogenesis and its comorbidities. The study involved 60 patients with plaque psoriasis and 30 healthy volunteers matched for gender, age, and BMI. Serum and urine samples were taken from the participants and tested for TRP, indoleamine 2,3-dioxygenase (IDO), 2,3-tryptophan dioxygenase (TDO), kynurenine (KYN), kynurenic acid (KYNA), quinolinic acid (QUIN), and numerous laboratory parameters. Correlations between the metabolites’ levels and clinical, laboratory parameters and depression occurrence were statistically evaluated. Concentrations of tryptophan, kynurenic acid, and quinolinic acid in serum and urine were significantly higher among patients with psoriasis (p < 0.05 and p < 0.001, p < 0.05 and p < 0.05 and p < 0.001 and p < 0.001, respectively). A significant stimulation of the kynurenine pathway in serum and urine of patients with psoriasis suggests its role in its pathogenesis and interplay between chronic inflammation or comorbidities. Further research is needed to discover whether the increase in KP metabolites is an indicator of inflammation or a compensatory mechanism in psoriasis. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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13 pages, 2340 KB

Open AccessArticle

Difamilast, a Topical Phosphodiesterase 4 Inhibitor, Produces Soluble ST2 via the AHR–NRF2 Axis in Human Keratinocytes

by Gaku Tsuji, Ayako Yumine, Koji Kawamura, Masaki Takemura, Makiko Kido-Nakahara, Kazuhiko Yamamura and Takeshi Nakahara

Int. J. Mol. Sci. 2024, 25(14), 7910; https://doi.org/10.3390/ijms25147910 - 19 Jul 2024

Cited by 6 | Viewed by 4723

Abstract

Difamilast, a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective in the treatment of atopic dermatitis (AD), although the mechanism involved remains unclear. Since IL-33 plays an important role in the pathogenesis of AD, we investigated the effect of difamilast on [...] Read more.

Difamilast, a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective in the treatment of atopic dermatitis (AD), although the mechanism involved remains unclear. Since IL-33 plays an important role in the pathogenesis of AD, we investigated the effect of difamilast on IL-33 activity. Since an in vitro model of cultured normal human epidermal keratinocytes (NHEKs) has been utilized to evaluate the pharmacological potential of adjunctive treatment of AD, we treated NHEKs with difamilast and analyzed the expression of the suppression of tumorigenicity 2 protein (ST2), an IL-33 receptor with transmembrane (ST2L) and soluble (sST2) isoforms. Difamilast treatment increased mRNA and protein levels of sST2, a decoy receptor suppressing IL-33 signal transduction, without affecting ST2L expression. Furthermore, supernatants from difamilast-treated NHEKs inhibited IL-33-induced upregulation of TNF-α, IL-5, and IL-13 in KU812 cells, a basophil cell line sensitive to IL-33. We also found that difamilast activated the aryl hydrocarbon receptor (AHR)–nuclear factor erythroid 2-related factor 2 (NRF2) axis. Additionally, the knockdown of AHR or NRF2 abolished the difamilast-induced sST2 production. These results indicate that difamilast treatment produces sST2 via the AHR–NRF2 axis, contributing to improving AD symptoms by inhibiting IL-33 activity. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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Review

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26 pages, 4422 KB

Open AccessReview

From Pathways to Patients in Atopic Dermatitis: Advanced Systemic Therapies

by Alvaro Prados-Carmona, Husein Husein-ElAhmed, Francisco José Navarro-Triviño and Ricardo Ruiz-Villaverde

Int. J. Mol. Sci. 2025, 26(23), 11487; https://doi.org/10.3390/ijms262311487 - 27 Nov 2025

Cited by 3 | Viewed by 3411

Abstract

Atopic dermatitis is the most prevalent chronic inflammatory skin disease, posing a significant individual and healthcare burden. Traditionally managed with topical agents and broad immunosuppressants, the treatment landscape has shifted significantly in recent years. This review explores the transition from immunopathogenic understanding to [...] Read more.

Atopic dermatitis is the most prevalent chronic inflammatory skin disease, posing a significant individual and healthcare burden. Traditionally managed with topical agents and broad immunosuppressants, the treatment landscape has shifted significantly in recent years. This review explores the transition from immunopathogenic understanding to personalized treatment strategies through advanced systemic therapies. We provide a thorough description of the current therapeutic arsenal, including approved monoclonal antibodies and Janus kinase (JAK) inhibitors, as well as experimental agents under clinical investigation. Key cytokines and receptors implicated in type 2 inflammation are explored alongside relevant intracellular signaling pathways. Special attention has been given to literature published from 2015 onwards. By synthesizing the latest scientific and clinical knowledge, this review aims to provide clinicians with practical guidance for navigating the evolving landscape of atopic dermatitis management and improving patient outcomes. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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16 pages, 885 KB

Open AccessReview

Molecular Mechanisms in the Etiopathology of Rosacea—Systematic Review

by Anastazja Andrusiewicz, Sofiia Khimuk, Daniel Mijas, Bohdan Shmorhun and Danuta Nowicka

Int. J. Mol. Sci. 2025, 26(23), 11292; https://doi.org/10.3390/ijms262311292 - 22 Nov 2025

Cited by 7 | Viewed by 2896

Abstract

Rosacea is a chronic inflammatory skin disorder of multifactorial pathogenesis, in which dysregulated innate immunity, neurovascular dysfunction, oxidative stress, and microbiome imbalance are central contributors. Recent molecular studies have revealed altered cytokine expression (e.g., IL-1β, IL-6, IL-36 family), aberrant activation of signaling pathways [...] Read more.

Rosacea is a chronic inflammatory skin disorder of multifactorial pathogenesis, in which dysregulated innate immunity, neurovascular dysfunction, oxidative stress, and microbiome imbalance are central contributors. Recent molecular studies have revealed altered cytokine expression (e.g., IL-1β, IL-6, IL-36 family), aberrant activation of signaling pathways (STAT3, NF-κB, MAPKs), and enhanced expression of innate immune receptors such as TLR2,b TLR4, and TLR7, all of which promote chronic inflammation, angiogenesis, and barrier dysfunction. This systematic review was performed according to PRISMA guidelines. A total of 1425 records were retrieved from PubMed, Scopus, and Web of Science, and 14 studies met the inclusion criteria. The included studies comprised both clinical cohorts and translational experimental investigations using human samples. Reported findings consistently confirmed systemic and tissue-specific inflammatory activity, with elevated circulating monocytes, indoleamine 2,3-dioxygenase, and inflammatory indices, as well as tissue expression of STAT3, NF-κB, MAPKs, and cathelicidin fragments. Oxidative stress markers (TOS, OSI, AOPP, MMP-9) and hypoxia-related molecules (HIF-1α) were significantly increased in patients, correlating with disease severity and vascular manifestations. Taken together, these results highlight that rosacea involves both cutaneous and systemic molecular alterations. The evidence identifies multiple biomarkers with diagnostic potential and provides mechanistic insights into immune, vascular, and metabolic dysregulation. Future research should aim to validate these findings in larger cohorts, establish standardized biomarker panels, and explore novel therapeutic strategies targeting key molecular pathways. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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19 pages, 340 KB

Open AccessReview

The Role of Selected Proteins in the Pathogenesis of Psoriasis

by Mateusz Matwiejuk, Agnieszka Kulczyńska-Przybik, Hanna Myśliwiec, Adrian Chabowski, Barbara Mroczko and Iwona Flisiak

Int. J. Mol. Sci. 2025, 26(13), 6475; https://doi.org/10.3390/ijms26136475 - 4 Jul 2025

Viewed by 2324

Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disease with complex genetic, environmental, and immunological determinants. Beyond the skin, it affects multiple systems, including the joints and cardiovascular system. A hallmark of psoriasis is an overactivation of the innate and adaptive immune responses, leading [...] Read more.

Psoriasis is a chronic, immune-mediated inflammatory skin disease with complex genetic, environmental, and immunological determinants. Beyond the skin, it affects multiple systems, including the joints and cardiovascular system. A hallmark of psoriasis is an overactivation of the innate and adaptive immune responses, leading to dysregulated cytokine signaling, altered keratinocyte function, and aberrant expression of structural and regulatory proteins. In recent years, growing attention has been given to the skin as a neuro–immuno–endocrine organ, with evidence showing the role of stress-related neuropeptides, UVB-induced immune modulation, and vitamin D signaling in the disease pathogenesis. This review highlights emerging evidence on key multifunctional proteins—elafin, chemerin, and NAMPT (visfatin)—that exert both pro- and anti-inflammatory actions. Although still underexplored, these molecules appear to contribute significantly to the psoriatic microenvironment by modulating inflammation, immunity, and skin barrier function. Their dual roles suggest complex interactions within the cutaneous immune–neuroendocrine network, positioning them as potential biomarkers or therapeutic targets in psoriasis. By integrating insights into classical and emerging mediators, this review aims to provide a comprehensive perspective on the evolving landscape of psoriasis pathophysiology. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

9 pages, 905 KB

Open AccessReview

The Carcinogenesis of the Human Scalp: An Immunometabolic-Centered View

by Baruch Kaplan, Rebecca von Dannecker and Jack L. Arbiser

Int. J. Mol. Sci. 2024, 25(22), 12064; https://doi.org/10.3390/ijms252212064 - 10 Nov 2024

Viewed by 2787

Abstract

The human scalp is a common site of skin cancer in humans, with nonmelanoma skin cancer being exceedingly common. In this review, two dermatologists with extensive experience in cutaneous oncology will discuss unique features of the epidemiology of cancer of the scalp. Clinical [...] Read more.

The human scalp is a common site of skin cancer in humans, with nonmelanoma skin cancer being exceedingly common. In this review, two dermatologists with extensive experience in cutaneous oncology will discuss unique features of the epidemiology of cancer of the scalp. Clinical observations on these common skin cancers lead to insight into the pathogenesis and potential prevention and treatment of cutaneous scalp neoplasia. Our hypothesis is that the presence of hair protects against the development of skin cancer but not by serving as a physical shield but rather by providing continuous IL-17-biased immunosurveillance. The loss of hair allows for a release from immunosurveillance, resulting in the expansion of neoplastic cells towards skin cancer. Both hair follicles and metabolic changes in stroma allow for permissiveness for tumor promotion. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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21 pages, 2018 KB

Open AccessReview

The Association between Genetics and Response to Treatment with Biologics in Patients with Psoriasis, Psoriatic Arthritis, Rheumatoid Arthritis, and Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis

by Rownaq Fares Al-Sofi, Mie Siewertsen Bergmann, Claus Henrik Nielsen, Vibeke Andersen, Lone Skov and Nikolai Loft

Int. J. Mol. Sci. 2024, 25(11), 5793; https://doi.org/10.3390/ijms25115793 - 26 May 2024

Cited by 21 | Viewed by 5928

Abstract

Genetic biomarkers could potentially lower the risk of treatment failure in chronic inflammatory diseases (CID) like psoriasis, psoriatic arthritis (PsA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). We performed a systematic review and meta-analysis assessing the association between single nucleotide polymorphisms (SNPs) [...] Read more.

Genetic biomarkers could potentially lower the risk of treatment failure in chronic inflammatory diseases (CID) like psoriasis, psoriatic arthritis (PsA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). We performed a systematic review and meta-analysis assessing the association between single nucleotide polymorphisms (SNPs) and response to biologics. Odds ratio (OR) with 95% confidence interval (CI) meta-analyses were performed. In total, 185 studies examining 62,774 individuals were included. For the diseases combined, the minor allele of MYD88 (rs7744) was associated with good response to TNFi (OR: 1.24 [1.02–1.51], 6 studies, 3158 patients with psoriasis or RA) and the minor alleles of NLRP3 (rs4612666) (OR: 0.71 [0.58–0.87], 5 studies, 3819 patients with RA or IBD), TNF-308 (rs1800629) (OR: 0.71 [0.55–0.92], 25 studies, 4341 patients with psoriasis, RA, or IBD), FCGR3A (rs396991) (OR: 0.77 [0.65–0.93], 18 studies, 2562 patients with psoriasis, PsA, RA, or IBD), and TNF-238 (rs361525) (OR: 0.57 [0.34–0.96]), 7 studies, 818 patients with psoriasis, RA, or IBD) were associated with poor response to TNFi together or infliximab alone. Genetic variants in TNFα, NLRP3, MYD88, and FcRγ genes are associated with response to TNFi across several inflammatory diseases. Most other genetic variants associated with response were observed in a few studies, and further validation is needed. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)

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