Experimental Dermatology最新文献

{"title":"Glycosylation in Dermatology: Unveiling the Sugar Coating of Skin Disease","authors":"Linxia Shen,&nbsp;Jui-Ming Lin,&nbsp;Jinran Lin,&nbsp;Wenyu Wu","doi":"10.1111/exd.70098","DOIUrl":"https://doi.org/10.1111/exd.70098","url":null,"abstract":"<p>Glycosylation is a common and complex post-translational modification (PTM) of proteins, involving the attachment of glycans under the regulation of various enzymes such as glycosyltransferases. Glycosylation facilitates the correct folding of peptide chains, modifies protein conformation and activity, enhances protein stability and influences inter-protein interactions. N-glycosylation and O-glycosylation are two prevalent forms, encompassing a wide range of modifications, including sialylation, fucosylation and galactosylation. In skin tumours, abnormal glycosylation promotes tumour cell proliferation, migration, invasion and metastasis, enhances anti-tumour immunity, and potentially affects immune checkpoint therapy. In inflammatory and autoimmune skin diseases, abnormal glycosylation in T and B lymphocyte subpopulations regulates antigen recognition, signal transduction, inflammatory factor secretion and immunoglobulin function, disrupting immune system homeostasis and impacting biologic therapy efficacy. Glycosylation correlates with the severity and activity of skin diseases, serving as a potential biomarker for diagnosis, condition assessment and prognosis determination. This review provides an overview of the role of protein glycosylation in melanoma, basal cell carcinoma, squamous cell carcinoma, psoriasis, systemic lupus erythematosus, dermatomyositis and skin aging. It analyses the biosynthetic process of glycosylation, elucidates functional changes in glycoproteins and their metabolism, and offers a theoretical basis for developing new targeted therapies.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143809787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Responses and Transcriptomic Analysis of Spesolimab in a Girl With Severe Dermatitis, Multiple Allergies and Metabolic Wasting Syndrome","authors":"Jinxiang Yang,&nbsp;Guofang Li,&nbsp;Yidong Tan,&nbsp;Bing Wang,&nbsp;Mingjun Lyu,&nbsp;Yijun Yang,&nbsp;Zhen Zhang,&nbsp;Yan Gu,&nbsp;ZhiRong Yao,&nbsp;Jianying Liang","doi":"10.1111/exd.70097","DOIUrl":"https://doi.org/10.1111/exd.70097","url":null,"abstract":"<div>\u0000 \u0000 <p>Severe dermatitis, multiple allergies, and metabolic wasting syndrome (SAM) is a rare inherited disorder caused by biallelic loss-of-function mutations in the desmoglein-1 (<i>DSG1</i>) or desmoplakin (<i>DSP</i>) genes. Previous studies have demonstrated that acitretin and systemic biologics targeting IL-17, IL-12/IL-23, and IL-4 are effective in treating SAM syndrome. We report the case of an 8-year-old girl diagnosed with SAM syndrome who suffered from recurrent rash episodes due to infections and achieved remission with a combination therapy of Spesolimab and acitretin. Comprehensive diagnostic workup, including serum inflammatory factor assays, flow cytometry, skin immunohistochemical staining, and skin RNA sequencing (RNA-seq), revealed elevated IL-36G levels in SAM syndrome, which may be associated with the pathogenesis of generalised pustular psoriasis (GPP) through shared IL-36-mediated mechanisms. This case highlights the therapeutic potential of targeting the IL-36 pathway in SAM syndrome and supports the use of skin RNA-seq for personalised selection of anti-inflammatory biologics in rare dermatological disorders. This report marks the first clinical application of Spesolimab in SAM syndrome, offering a novel therapeutic approach.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143809376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Off-Label Use of Topical Ruxolitinib in Dermatology: A Systematic Literature Review and Current Perspectives","authors":"Marco Spadafora,&nbsp;Serena Morsia,&nbsp;Vito Giuseppe Di Lernia,&nbsp;Shaniko Kaleci,&nbsp;Giovanni Pellacani,&nbsp;Caterina Longo","doi":"10.1111/exd.70095","DOIUrl":"https://doi.org/10.1111/exd.70095","url":null,"abstract":"<p>JAK inhibitors are used to treat various inflammatory skin diseases. However, systemic formulations are associated with an increased risk of major adverse events. Ruxolitinib 1.5% cream is a selective topical JAK1 and JAK2 inhibitor, which has recently been approved by EMA and MHRA for treating non-segmental vitiligo, while being FDA-approved for both vitiligo and atopic dermatitis. Recent literature has reported the off-label use of topical Ruxolitinib for several skin conditions, but data are mostly limited to single case reports and series and few prospective studies, with mixed results. We conducted a systematic review of the literature to investigate the potential efficacy of topical Ruxolitinib in various skin diseases in an off-label setting. The following keywords were used for searching the MEDLINE (Pubmed) and Scopus databases from inception to September 2024: “ruxolitinib cream and dermatology” and “topical ruxolitinib and dermatology”. Reviews, articles not focusing on the main topic, books and book chapters, and articles with no English text were excluded. A total of 170 studies were screened, of which 112 fell within exclusion criteria and 58 were assessed for eligibility. Of these, 28 studies, published between 2012 and 2024, were selected. Ruxolitinib cream resulted in being used off-label mostly for treating lichenoid and granulomatous dermatoses, as well as alopecia areata. While for the former skin conditions, topical ruxolitinib proved to be effective and safe, results on efficacy in alopecia areata were controversial. Topical ruxolitinib might be a promising therapeutic option for lichenoid and granulomatous dermatoses. Noteworthily, despite the exciting results from the oral formulation, no consistent data were described for topical ruxolitinib in alopecia areata. Our review reported encouraging results for many inflammatory skin conditions that should be investigated in further studies.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143786891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Neutrophil Activation in Psoriatic Skin at Relapse Following Dead Sea Climatotherapy","authors":"Thomas Emmanuel,&nbsp;Hakim Ben Abdallah,&nbsp;Elena Baez,&nbsp;Ida Maja Rather,&nbsp;Torben Steiniche,&nbsp;Anne Bregnhøj,&nbsp;Lars Iversen,&nbsp;Claus Johansen","doi":"10.1111/exd.70094","DOIUrl":"https://doi.org/10.1111/exd.70094","url":null,"abstract":"<p>Psoriasis, a chronic inflammatory skin disorder characterised by erythematous and scaly plaques, can be both physically and emotionally distressing for patients. Dead Sea climatotherapy (DSC), a treatment modality combining sun exposure, mineral-rich water and mud therapy during 4 weeks at Ein Gedi, Israel, is used for a small group of patients with psoriasis. This study aimed to investigate the cellular composition of psoriatic skin lesions at relapse after complete clearance from DSC. Skin biopsies from baseline, end of treatment and relapse were collected from eight patients with plaque psoriasis who achieved complete clearance from Dead Sea climatotherapy treatment. These biopsies were subjected to immunohistochemistry, RNA sequencing and quantitative polymerase chain reaction analysis (qPCR). Our findings demonstrate that DSC effectively reduces inflammatory markers to levels comparable to baseline non-lesional skin in the short term. The differential expression analysis identified several upregulated differentially expressed genes, including <i>OSM</i>, <i>CXCL8</i>, <i>TREM1</i>, <i>CXCL1</i>, <i>CSF3R</i>, <i>BCL2A1</i> and <i>CXCL2</i>, in relapsed psoriasis skin compared with baseline lesional skin. These findings were confirmed by qPCR analysis. Pathway enrichment analysis indicated a marked upregulation of neutrophil-associated pathways in relapse skin compared with baseline lesional skin. Immunohistochemical staining for neutrophil markers, such as CD11b, CD15, CD66b, CD207, MPO and NE, showed a non-significant trend towards enhanced neutrophil infiltration and activation at relapse. In conclusion, while DSC provides short-term effectiveness in managing psoriasis, the initial relapse phase is associated with neutrophil activation and migration. Thus, targeting neutrophils early in the psoriasis disease course may disturb the evolution of psoriasis, potentially preventing disease chronicity.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143770369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Strong Is the Link Between Merkel Cell Carcinoma and the Occurrence of Other Skin Cancer Types? A Meta-Analysis","authors":"Trairong Chokwassanasakulkit,&nbsp;Nigel A. J. McMillan","doi":"10.1111/exd.70092","DOIUrl":"https://doi.org/10.1111/exd.70092","url":null,"abstract":"<p>This meta-analysis presents findings from nine studies involving 4626 cases of primary Merkel cell carcinoma (MCC), aimed at evaluating the relationship between primary MCC and the incidence of a second skin cancer. The analysis reveals a significant association, with a calculated risk ratio of 2.97 (95% CI, 1.70–5.19, <i>p</i> = 0.0001), indicating that individuals diagnosed with primary MCC are nearly three times more likely to develop the second skin cancer compared to patients with other second cancers. Among the second skin cancers analysed, basal cell carcinoma (BCC) showed the highest risk (0.69, 95% CI 0.35–1.37), followed by squamous cell carcinoma (SCC) (0.45, 95% CI 0.23–0.90) and melanoma (0.31, 95% CI 0.19–0.50). While geographic analysis showed that patients in Northern Europe have a non-significant 1.7-fold increased likelihood of developing the second skin cancer relative to those in North America (USA), where the likelihood of developing the second skin cancer is significantly lower at 0.7 times. The results underscore the importance of implementing enhanced surveillance and preventive strategies for individuals at increased risk. By identifying these associations, we may improve the early detection of the second skin cancer in patients with MCC.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70092","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “The Dynamics of Circulating Tumour DNA (ctDNA) During Treatment Reflects Tumour Response in Advanced Melanoma Patients”","authors":"","doi":"10.1111/exd.70091","DOIUrl":"https://doi.org/10.1111/exd.70091","url":null,"abstract":"<p>L. Di Nardo, L. Del Regno, A. Di Stefani, et al., “The dynamics of circulating tumour DNA (ctDNA) during treatment reflects tumour response in advanced melanoma patients,” Experimental Dermatology 32 (2023):1785–1793.</p><p>In the article, the author, Yelinay Alpay, was added as co-author to aknowledge her involvement in the project .</p><p>The correct list of authors and affiliations should read:</p><p><b>Lucia Di Nardo</b>^<b>1</b> <b>| Laura Del Regno</b>^<b>2</b> <b>| Alessandro Di Stefani</b>^<b>2</b> <b>| Maria Mannino</b>^<b>2</b> <b>| Barbara Fossati</b>^<b>2</b> <b>| Silvia Catapano</b>^<b>2</b> <b>| Laura Quattrini</b>^<b>2</b> <b>|Yelinay Alpay</b>^<b>13</b> <b>|Cristina Pellegrini</b>^<b>3</b> <b>| Alessio Cortellini</b>^<b>4,5</b> <b>| Alessandro Parisi</b>^<b>6,7</b> <b>| Ettore Capoluongo</b>^{<b>8,9,10</b>} <b>| Chiara Autilio</b>^<b>11</b> <b>| Maria Concetta Fargnoli</b>^<b>3,12</b> <b>| Ketty Peris</b>^<b>1,2</b></p><p>¹Dermatologia, Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Rome, Italy</p><p>²UOC di Dermatologia, Dipartimento di Scienze Mediche e Chirurgiche, Fondazione Policlinico Universitario A, Gemelli –IRCCS, Rome, Italy.</p><p>³Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy</p><p>⁴Medical Oncology Unit, Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy.</p><p>⁵Department of Surgery &amp; Cancer, Imperial College London, London, UK</p><p>⁶Department of Oncology, Università Politecnica delle Marche, Azienda Ospedaliero-Universitaria Ospedali Riuniti di Ancona, Ancona, Italy</p><p>⁷Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy</p><p>⁸Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Federico II, Naples, Italy</p><p>⁹CEINGE, Advanced Biotechnology, Naples, Italy</p><p>¹⁰Department of Clinical Pathology and Genomics, Ospedale Cannizzaro, Catania, Italy</p><p>¹¹Department of Biochemistry and Molecular Biology and Research Institute Hospital, Complutense University, Madrid, Spain</p><p>¹²Dermatology Unit, San Salvatore Hospital, L'Aquila, Italy</p><p>¹³Salisbury NHS Foundation Trust, Salisbury, UK</p><p>The online version of the article has been corrected.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperuricemia Exacerbates Psoriatic Inflammation by Inducing M1 Macrophage Activation and Th1 Cell Differentiation","authors":"Shu-Yi Wei,&nbsp;Shuang He,&nbsp;Xiao-Yan Wu,&nbsp;Yan Zhang,&nbsp;Ying-Ping Xu,&nbsp;Bin Yang,&nbsp;Yu-Zhe Sun","doi":"10.1111/exd.70090","DOIUrl":"https://doi.org/10.1111/exd.70090","url":null,"abstract":"<div>\u0000 \u0000 <p>A higher prevalence of hyperuricemia is observed in psoriasis, yet the precise involvement of hyperuricemia in psoriasis remains unclear. Therefore, we investigated the relationship between hyperuricemia and psoriasis, as well as the potential mechanisms through which hyperuricemia may promote psoriatic inflammation. Firstly, a literature review on psoriasis and serum uric acid (SUA) levels and a retrospective analysis on PASI scores and SUA of 147 psoriasis patients at the Dermatology Hospital of Southern Medical University were performed. Then mouse models of hyperuricemia and psoriasis were established to assess the impact of hyperuricemia on psoriasis. Finally, assays examined monosodium urate (MSU) on macrophage M1 polarisation, Th1 differentiation and expressions of NLRP3 and ASC. The literature review indicated inconsistent SUA-psoriasis links; however, our clinical data indicated a positive correlation between PASI scores and SUA. Mouse model results indicated that hyperuricemia exacerbated psoriatic lesions and upregulated the transcription of inflammatory cytokines (IL-17A, IL-17F, IL-23A, IL-8, TNF-α and IL-1β) in skin lesions, effects which were reversed with allopurinol treatment. GO-BP, KEGG and GSEA enrichment analyses of RNA-seq data from mice skin lesions and spleens revealed increased enrichment of Toll-like receptor pathways, TNF-α signalling pathways and innate immune cell migration pathways. CIBERSORTx analysis showed increased M1 cell infiltration in skin lesions and Th1 differentiation in splenic lymphocytes under hyperuricemic conditions. In vitro, MSU enhanced IMQ or LPS-induced macrophage M1 polarisation and Th1 differentiation when co-cultured with M1 cells, which depends on TLR4 expression. In conclusion, hyperuricemia may exacerbate psoriasis by promoting macrophage M1 polarisation, increasing Th1 differentiation and psoriatic inflammation.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of RCC2 as a Risk Gene Associated With Basal Cell Carcinoma and Experimental Validation","authors":"Yu Zhang,&nbsp;Xu Han,&nbsp;Jiayan Ren,&nbsp;Man Zhu,&nbsp;Dake Chu,&nbsp;Yanmin Zhang,&nbsp;Qi Su,&nbsp;Zixi Zhang","doi":"10.1111/exd.70082","DOIUrl":"https://doi.org/10.1111/exd.70082","url":null,"abstract":"<div>\u0000 \u0000 <p>Basal cell carcinoma (BCC) is a common type of skin cancer that is increasing in prevalence worldwide. Previous genome-wide association studies (GWAS) have identified certain genetic loci associated with BCC. However, many potential disease-causing genes of BCC remain to be discovered. While the sonic hedgehog (SHH) signalling pathway and mutations in PTCH1/2 and SMO are well-established drivers of BCC pathogenesis, novel genetic factors may complement existing therapeutic targets such as vismodegib and sonidegib. The Mendelian Randomization (MR) study used multiple omics datasets including expression quantitative trait loci (eQTL), methylation quantitative trait loci (mQTL), and protein quantitative trait loci (pQTL) to identify genetic factors associated with an increased risk of developing BCC. Transcriptome analysis of the GEO database then verified the specific expression of key genes. In addition, in vitro experiments were used to silence the key gene to observe the effect of this gene on the proliferation ability of A431 cells. Combined with the multi-omics MR Analysis results, six CpG sites were identified with the RCC2 gene associated with BCC risk. Additionally, single-cell transcriptome analysis confirmed the specific expression of RCC2 in the BCC cohort. In the in vitro validation experiment, siRCC2-1/2 was transfected into the A431 cells, significantly decreasing the expression of RCC2 in the cells. Moreover, the proliferation of A431 cells was significantly inhibited after RCC2 was knocked down. We identified a risk gene RCC2 associated with BCC by MR-based bioinformatics analysis and demonstrated that inhibition of RCC2 inhibited the proliferation of A431 in vitro. These findings provide new strategies for targeted therapy of BCC.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaphorin 7a Regulates the Expression of IL-4 and IL-33 in a Cell Model of Atopic Dermatitis and Is Associated With Disease Severity","authors":"Mindy Ming-Huey Guo,&nbsp;Kuang-Den Chen,&nbsp;Ho-Chang Kuo","doi":"10.1111/exd.70087","DOIUrl":"https://doi.org/10.1111/exd.70087","url":null,"abstract":"<div>\u0000 \u0000 <p>Neuroimmune interaction is crucial to inducing pruritic sensations in atopic dermatitis (<span>AD</span>). In this study, we examine the neuroimmune pathways involved in children with <span>AD</span>. HumanMethylation450 BeadChip and GeneChip Human Transcriptome Array 2.0 from 24 children with <span>ad</span> and 24 healthy controls were cross-referenced with gene expression data from GSE116486. <i>SEMA7A</i>, which encodes for semaphorin 7a and is associated with neuron development and immune response and was identified on pathway analysis as a crucial gene in children with <span>ad</span>. In addition, we found that <i>SEMA7A</i> cytosine-phosphate-guanine sites (CpG sites) cg13557411 and cg17917837 were hypomethylated, and mRNA expression of <i>SEMA7A</i> was higher in children with <span>ad</span>. Vectors containing <i>SEMA7A</i> were then transfected into Jurkat T cells, which increased the protein excretion of interleukin 4 (IL-4) and the mRNA expression of interleukin 1 receptor-like 1 (IL1RL1, receptor for the cytokine IL-33). Furthermore, stimulation of HaCaT keratinocytes with SEMA7A protein resulted in increased mRNA expression of the genes interleukin 33 (<i>IL33</i>) and <i>IL1RL1</i>, but suppressed mRNA expression of the tight junction protein ZO-1(<i>TJP1</i>). In conclusion, in this study, we found that <i>SEMA7A</i> is overexpressed in patients with AD and is a central gene on pathway analysis. Results of our study suggest that overexpression of <i>SEMA7A</i> is associated with increased expression of <i>IL4, IL33</i> and its receptor <i>IL1RL1</i>, which are associated with pruritic sensation in AD. <i>SEMA7A</i> also appears to suppress the expression of <i>TJP1</i> in keratinocytes, thereby possibly increasing the permeability of the skin barrier. <i>SEMA7A</i> may be an alternative therapeutic target in <span>AD</span>, especially for neuroimmune-related pruritis.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Emissions From Oriented Strand Board on the Development of Atopic Dermatitis Using Two Different Experimental Mouse Models","authors":"Evelyn Schneider,&nbsp;Katja Butter,&nbsp;Benjamin Schnautz,&nbsp;Stephanie Musiol,&nbsp;Johanna Grosch,&nbsp;Sonja Schindela,&nbsp;Manuel Garcia-Käufer,&nbsp;Richard Gminski,&nbsp;Stefan Haak,&nbsp;Martin Ohlmeyer,&nbsp;Carsten B. Schmidt-Weber,&nbsp;Stefanie Eyerich,&nbsp;Julia Esser-von Bieren,&nbsp;Francesca Alessandrini","doi":"10.1111/exd.70086","DOIUrl":"10.1111/exd.70086","url":null,"abstract":"<p>Atopic dermatitis (AD) is an allergic skin disease widespread in children, which later in life can predispose them to asthma. Oriented strand board (OSB), increasingly used in the construction industry, emits volatile organic compounds in the indoor air, some of which may exacerbate <span>AD</span> development in humans. The aim of this study was to evaluate the effects of OSB emissions on the development of AD and lung inflammation. Two different murine <span>AD</span> models, induced by calcipotriol or oxazolone, were exposed to higher- or lower-emitting OSB throughout the experiments. Physiological, biochemical, and immunological parameters of skin disease development, as well as lung inflammatory parameters, were evaluated. Exposure to higher-emitting OSB, characterised especially by high 3-carene emissions, exacerbated some parameters of <span>AD</span>, such as skin barrier function and thickness, with accumulation of eosinophils and 15-lipoxygenase (15-LOX)-driven mediators in both models, whereas IL-4 or 5-LOX-positive cells were increased in only the calcipotriol or oxazolone model, respectively. In the lungs of calcipotriol-treated mice, higher-emitting OSB increased lung eosinophil recruitment. Exposure to lower-emitting OSB had no or even beneficial effects on the skin or lungs of murine <span>AD</span> models. 3-carene in OSB emissions, alone or in combination with other substances, may promote the development of <span>AD</span> and prime the lungs towards an allergic phenotype. Identification and quantification of potentially harmful emitting sources in indoor air may be important for <span>AD</span> prevention or control.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"34 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}