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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: 25 February 2026 | Viewed by 10552

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Special Issue Editor

Dr. Nabiha Yusuf

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Guest Editor

Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: interferons; cancer; innate immunity; adaptive immunity; skin; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skin inflammation is a general term for skin inflammatory diseases caused by various internal and external infections or non-infectious factors, typically characterized by itchiness, redness, and a rash.

In this Special Issue, we focus on the molecular-level research of skin inflammation, especially the current molecular mechanism, diagnosis, and treatment of skin inflammation. At the same time, for several types of inflammatory skin diseases, including psoriasis, hidradenitis suppurativa, acne, rosacea, atopic dermatitis, contact dermatitis, stasis dermatitis, and seborrheic dermatitis, this Special Issue will also focus on their molecular pathogenesis and major breakthroughs in treatment. For this Special Issue, we welcome original research and review articles relating to skin infections and inflammation and hope that the proposed theme will be of great interest to the scientific community.

Dr. Nabiha Yusuf
Guest Editor

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Keywords

skin inflammation
molecular diagnosis
dermatitis
molecular pathogenesis

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Published Papers (6 papers)

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Research

Jump to: Review

12 pages, 2006 KB

Open AccessArticle

Resilience of the Skin Microbiome in Atopic Dermatitis During Short-Term Topical Treatment

by Malin Glindvad Ahlström, Rie Dybboe Bjerre, Yue Hu, Maike Seifert, Fredrik Boulund, Lone Skov, Jeanne Duus Johansen and Lars Engstrand

Int. J. Mol. Sci. 2025, 26(23), 11737; https://doi.org/10.3390/ijms262311737 - 4 Dec 2025

Viewed by 761

Abstract

Atopic dermatitis (AD) is associated with microbial dysbiosis and impaired skin barrier function. Topical therapies, such as moisturisers and antimicrobial fragrance compounds, may modulate the skin microbiome and support disease management. The objective was to evaluate how a moisturiser and a fragrance compound (farnesol) influence skin microbiome composition in individuals with AD and healthy controls. In a randomised, controlled, operator-blinded study, 15 AD patients and 15 healthy controls applied a moisturiser, farnesol, moisturiser + farnesol, or no treatment to defined skin areas over 7 days. Microbiome composition, alpha/beta diversity, and core taxa were analysed using shotgun metagenomics. At baseline, AD patients exhibited distinct microbial profiles, including elevated Staphylococcus aureus and Micrococcus luteus. Neither moisturiser nor farnesol significantly altered richness, beta diversity, or core taxa in either AD patients or controls. However, moisturiser use in healthy individuals modestly increased Shannon diversity, reflecting improved microbial evenness. Despite clear microbiome differences between AD and healthy skin, short-term topical treatment did not markedly shift microbial composition. The observed stability underscores the resilience of the skin microbiome and suggests that longer interventions or more targeted formulations may be necessary to influence microbial dysbiosis in AD. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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16 pages, 3389 KB

Open AccessArticle

Elevated Serum Levels of miRNA-155 in Children with Atopic Dermatitis: A Potential Biomarker of Disease

by Natalia Gołuchowska, Aldona Ząber, Sylwia Walczewska, Agata Będzichowska, Klaudia Brodaczewska, Aleksandra Majewska, Bolesław Kalicki and Agata Tomaszewska

Int. J. Mol. Sci. 2025, 26(19), 9689; https://doi.org/10.3390/ijms26199689 - 4 Oct 2025

Cited by 1 | Viewed by 824

Abstract

Atopic dermatitis (AD) is the most common inflammatory skin disease in the pediatric population. In recent years, the role of microRNAs in inflammatory and immunological mechanisms as specific biomarkers of AD has received growing attention. The aim of the present study was a quantitative assessment of serum expression levels of miR-100, miR-224 and miR-155 in children with AD compared with healthy peers, and an analysis of their potential associations with clinical disease phenotype, severity of skin lesions (SCORAD), cytokine profile, immunological parameters and the presence of concomitant allergic diseases. The study included 12 children with AD and 9 healthy children. Selected miRNAs were isolated from serum, followed by reverse transcription using universal primers and quantification by qRT-PCR. Children with AD exhibited significantly higher expression levels of miR-155 compared with controls (p = 0.003). No statistically significant differences were observed for miR-100 and miR-224. miR-100 expression was significantly higher in children with a positive history of inhalant allergy compared with those without such a diagnosis (p = 0.014). A positive correlation was observed between miR-100 levels and the percentage of eosinophils (r = 0.599; p = 0.052) as well as absolute eosinophil count (r = 0.600; p = 0.051). MiR-155 is significantly upregulated in children with AD suggesting it as a candidate biomarker worthy of further investigation in larger cohorts. Although miR-100 did not differentiate the groups, its correlation with eosinophilia and inhalant allergy suggests a role in disease phenotyping. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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14 pages, 3154 KB

Open AccessArticle

Downregulation of Mitophagy, Complex I Biogenesis, and Signaling by ROBO Receptors—Implications for Psoriasis Pathogenesis

by Malin Assarsson, Jan Söderman, Olaf Dienus and Oliver Seifert

Int. J. Mol. Sci. 2025, 26(12), 5546; https://doi.org/10.3390/ijms26125546 - 10 Jun 2025

Viewed by 1086

Abstract

The pathogenesis of psoriasis is complex and many specific immunopathogenic mechanisms still remain unclear. Our goal was to identify novel pathways involved in the pathogenesis of psoriasis by analyzing differentially expressed genes, and to conduct pathway and cluster analysis by comparing lesional and non-lesional skin with healthy controls. Accordingly, 2 mm punch biopsies were taken from lesional elbow skin and non-affected adjacent skin of 23 patients with plaque-type psoriasis and from the elbow skin of 25 healthy controls. Differentially expressed genes were analyzed through RNA sequencing, and gene set enrichment analysis was used to analyze biological pathways. Our results showed downregulation of the pathway clusters “Mitophagy” and “Respiratory Electron Transport” when comparing both lesional and non-lesional skin to control skin. The pathway “Signaling by ROBO receptors” was downregulated in all three comparisons. Conversely, pathways relating to SUMOylation were upregulated when comparing lesional skin to both non-lesional and control skin, and those relating to the synthesis of PIPs at the early endosome membrane were found to be upregulated in lesional skin compared to control skin. The dysregulation of pathways relating to mitophagy (involved in the removal of damaged mitochondria), complex I biogenesis (a component of the mitochondrial respiratory chain), signaling by ROBO receptors (important for cell migration), and the synthesis of PIPs at the early endosome membrane (with a pivotal role in endocytic pathways and autophagy) suggests their potential role in psoriasis. Further research into the mechanisms of these dysregulated pathways, along with confirmation of protein expression levels, is necessary to validate their roles in psoriasis pathogenesis. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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15 pages, 3500 KB

Open AccessArticle

The Relationship Between Neutrophil-to-Lymphocyte Ratio, Platelet-to-Lymphocyte Ratio, and Systemic Immune-Inflammation Index Markers and Response to Biological Therapy in Patients with Psoriasis

by Agnieszka Kimak-Pielas, Ewa Robak, Radosław Zajdel and Agnieszka Żebrowska

Int. J. Mol. Sci. 2025, 26(8), 3868; https://doi.org/10.3390/ijms26083868 - 19 Apr 2025

Cited by 3 | Viewed by 3831

Abstract

Plaque psoriasis is a chronic, immune-mediated inflammatory skin disease characterized by the formation of thick, scaly plaques. The disease is driven by dysregulation of the immune response, primarily involving T-helper cells, which create a persistent inflammatory environment. In recent years, several biomarkers reflecting systemic inflammation have been identified, including indices derived from a complete blood count, such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Systemic Immune-Inflammation Index (SII). The aim of our study was to explore the role of these markers in patients with psoriasis undergoing biological treatment. Medical records of 159 patients with plaque psoriasis receiving biologics were retrospectively reviewed. The NLR, PLR, and SII values were calculated from the hemograms of the patients. Additionally, demographic and psoriasis severity data were analyzed. During the 18-month follow-up, the mean NLR, PLR, SII, and CRP values were significantly decreased in comparison to the baseline (p < 0.05). No significant differences between anti-TNF, anti-IL-12/23, anti-IL-17, and anti-IL-23 drugs were identified (p > 0.05). The initial values of NLR, PLR, and SII were positively correlated with psoriasis severity. No relationship between the analyzed biomarkers and age, sex, psoriasis duration, and prior exposure to biological drugs was identified. CBC-derived biomarkers may be useful for monitoring inflammation reduction in psoriasis patients treated with biological drugs. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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18 pages, 34503 KB

Open AccessArticle

Corydalis Tuber Extract Alleviates Atopic Dermatitis: Transcriptomics-Based Mechanism Prediction and In Vitro/In Vivo Studies

by Seong-Eun Jin, Chang-Seob Seo, Woo-Young Jeon, Yong-Jin Oh, Hyeun-Kyoo Shin and Hyekyung Ha

Int. J. Mol. Sci. 2025, 26(3), 1291; https://doi.org/10.3390/ijms26031291 - 3 Feb 2025

Viewed by 2167

Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by recurrent eczema and chronic itching, affecting a significant portion of the global population. This study investigated the effects of Corydalis Tuber 70% ethanol extract (CTE) on tumor necrosis factor-α- and interferon-γ (TI)-stimulated human keratinocytes (HaCaT) and a house dust mite-induced AD mouse model, elucidating its mechanism via transcriptome analysis. A total of 13 compounds, including columbamine, corydaline, dehydrocorydaline, and glaucine, were identified in CTE using ultra performance liquid chromatography-tandem mass spectrometry. CTE downregulated pathways related to cytokine signaling and chemokine receptors in TI-stimulated HaCaT cells. It significantly inhibited C-C motif chemokine ligand (CCL)5, CCL17, and CCL22 levels by blocking the Janus kinase-signal transducers and activators of transcription and nuclear factor kappa-light-chain-enhancer of activated B cells pathways. In the AD mouse model, topical CTE significantly decreased dermatitis scores, epidermal thickening, and inflammatory cell infiltration. Plasma levels of histamine, immunoglobulin E, CCL17, CCL22, corticosterone, and cortisol were reduced. Lesions showed decreased thymic stromal lymphopoietin, CD4⁺ T cells, interleukin-4, and intercellular adhesion molecule-1 expression. The findings demonstrate that CTE alleviates AD by modulating inflammatory mediators, cytokines, and chemokines, reducing inflammatory cell infiltration, and alleviating stress-related factors. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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Review

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20 pages, 338 KB

Open AccessReview

Autoimmune Diseases of the Eyelid Skin: Molecular Pathways, Clinical Manifestations, and Therapeutic Insights

by Wojciech Luboń, Małgorzata Luboń, Monika Sarnat-Kucharczyk, Mariola Dorecka and Dorota Wyględowska-Promieńska

Int. J. Mol. Sci. 2025, 26(23), 11730; https://doi.org/10.3390/ijms262311730 - 4 Dec 2025

Viewed by 710

Abstract

The eyelid skin represents a unique anatomical and immunological interface between the external environment and the ocular surface. Due to its structural delicacy, dense vascularization, and continuous exposure to microbial and environmental antigens, it is a primary target of inflammatory and autoimmune processes. This review aims to synthesize current molecular insights into eyelid skin inflammation, with particular emphasis on autoimmune mechanisms. We discuss autoimmune diseases such as ocular cicatricial pemphigoid, pemphigus, discoid and systemic lupus erythematosus, and thyroid-associated orbitopathy, focusing on the roles of T helper cell subsets, pro-inflammatory cytokines (IL-1β, IL-6, IL-17, TNF-α), and autoantibody-mediated complement activation. We further address the contribution of the periocular microbiome and meibomian gland dysfunction. Diagnostic advances, including confocal microscopy, in vivo molecular imaging, and tear proteomics, are highlighted alongside emerging targeted therapies such as biologics and small molecules directed at IL-17, TNF-α, and B-cell activity. Finally, we propose future perspectives for precision medicine approaches, integrating omics technologies and microbiome-based therapies to advance personalized management of eyelid skin inflammation. Full article

(This article belongs to the Special Issue Molecular Research on Skin Inflammation)

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