Journal of dermatological science最新文献

{"title":"Maximizing the potential of biobanks in dermatology research","authors":"","doi":"10.1016/j.jdermsci.2024.03.003","DOIUrl":"10.1016/j.jdermsci.2024.03.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 2","pages":"Pages 98-99"},"PeriodicalIF":4.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140268281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated tryptophan metabolism and AhR pathway contributed to CXCL10 upregulation in stable non-segmental vitiligo","authors":"","doi":"10.1016/j.jdermsci.2024.06.003","DOIUrl":"10.1016/j.jdermsci.2024.06.003","url":null,"abstract":"<div><h3>Background</h3><p>Tryptophan metabolism dysregulation has been observed in vitiligo. However, drawing a mechanistic linkage between this metabolic disturbance and vitiligo pathogenesis remains challenging.</p></div><div><h3>Objective</h3><p>Aim to reveal the characterization of tryptophan metabolism in vitiligo and investigate the role of tryptophan metabolites in vitiligo pathophysiology.</p></div><div><h3>Methods</h3><p>LC-MS/MS, dual-luciferase reporter assay, ELISA, qRT-PCR, small interfering RNA, western blotting, and immunohistochemistry were employed.</p></div><div><h3>Results</h3><p>Kynurenine pathway activation and KYAT enzyme-associated deviation to kynurenic acid (KYNA) in the plasma of stable non-segmental vitiligo were determined. Using a public microarray dataset, we next validated the activation of kynurenine pathway was related with inflammatory-related genes expression in skin of vitiligo patients. Furthermore, we found that KYNA induced CXCL10 upregulation in keratinocytes <em>via</em> AhR activation. Moreover, the total activity of AhR agonist was increased while the AhR concentration <em>per se</em> was decreased in the plasma of vitiligo patients. Finally, higher KYAT, CXCL10, CYP1A1 and lower AhR expression in vitiligo lesional skin were observed by immunohistochemistry staining.</p></div><div><h3>Conclusion</h3><p>This study depicts the metabolic and genetic characterizations of tryptophan metabolism in vitiligo and proposes that KYNA, a tryptophan-derived AhR ligand, can enhance CXCL10 expression in keratinocytes.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Pages 33-41"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141494685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LEKTI domain 6 displays anti-inflammatory action in vitro and in a murine atopic dermatitis model","authors":"","doi":"10.1016/j.jdermsci.2024.03.004","DOIUrl":"10.1016/j.jdermsci.2024.03.004","url":null,"abstract":"<div><h3>Background</h3><p>Lympho-epithelial Kazal-type-related inhibitor (LEKTI) is a serine protease inhibitor consisting of multiple domains. A loss of function mutation is described in Netherton patients that show severe symptoms of atopic lesions and itch.</p></div><div><h3>Objectives</h3><p>LEKTI domain 6 (LD6) has shown strong serine protease-inhibitory action in <em>in vitro</em> assays and thus it was tested <em>in vitro</em> and <em>in vivo</em> for potential anti-inflammatory action in models of atopic skin disease.</p></div><div><h3>Methods</h3><p>Human skin equivalents were treated with LD6 and an inflammatory reaction was challenged by kallikrein-related endopeptidase 5 (KLK5). Furthermore, LD6 was tested on dorsal root ganglia cells stimulated with KLK5, SLIGRL and histamine by calcium imaging. The effect of topically administered LD6 (0.4–0.8%) in lipoderm was compared to a topical formulation of betamethasone-diproprionate (0.1%) in a therapeutic setting on atopic dermatitis-like lesions in NC/Nga mice sensitized to house dust mite antigen. Endpoints were clinical scoring of the mice as well as determination of scratching behaviour.</p></div><div><h3>Results</h3><p>KLK5 induced an upregulation of CXCL-8, CCL20 and IL-6 in skin equivalents. This upregulation was reduced by pre-incubation with LD6. KLK5 as well as histamine induced calcium influx in a population of neurons. LD6 significantly reduced the calcium response to both stimuli. When administered onto lesional skin of NC/Nga mice, both LD6 and betamethasone-dipropionate significantly reduced the inflammatory reaction. The effect on itch behaviour was less pronounced.</p></div><div><h3>Conclusion</h3><p>Topical administration of LD6 might be a new therapeutic option for treatment of lesional atopic skin.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Pages 13-20"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000501/pdfft?md5=f8c0be6d25d62f1e26d970990ec01145&pid=1-s2.0-S0923181124000501-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140156275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histological and molecular restoration of type VII collagen in Recessive dystrophic epidermolysis bullosa mouse skin by topical injection of keratinocyte-like cells differentiated from human adipose-derived mesenchymal stromal cells","authors":"","doi":"10.1016/j.jdermsci.2024.05.004","DOIUrl":"10.1016/j.jdermsci.2024.05.004","url":null,"abstract":"<div><h3>Background</h3><p>Recessive dystrophic epidermolysis bullosa (RDEB) is a severe skin fragility disorder caused by mutations in the <em>COL7A1</em> gene, which encodes type VII collagen (COL7), the main constituent of anchoring fibrils for attaching the epidermis to the dermis. Persistent skin erosions frequently result in intractable ulcers in RDEB patients. Adipose-derived mesenchymal stromal cells (AD-MSCs) are easily harvested in large quantities and have low immunogenicity. Therefore, they are suitable for clinical use, including applications involving allogeneic cell transplantation. Keratinocyte-like cells transdifferentiated from AD-MSCs (KC-AD-MSCs) express more COL7 than undifferentiated AD-MSCs and facilitate skin wound healing with less contracture. Therefore, these cells can be used for skin ulcer treatment in RDEB patients.</p></div><div><h3>Objective</h3><p>We investigated whether KC-AD-MSCs transplantation ameliorated the RDEB phenotype severity in the grafted skin of a RDEB mouse model (<em>col7a1</em>-null) on the back of the immunodeficient mouse.</p></div><div><h3>Methods</h3><p>KC-AD-MSCs were intradermally injected into the region surrounding the skin grafts, and this procedure was repeated after 7 days. After a further 7-day interval, the skin grafts were harvested.</p></div><div><h3>Results</h3><p>Neodeposition of COL7 and generation of anchoring fibrils at the dermal-epidermal junction were observed, although experiments were based on qualitative.</p></div><div><h3>Conclusion</h3><p>KC-AD-MSCs may correct the COL7 insufficiency, repair defective/reduced anchoring fibrils, and improve skin integrity in RDEB patients.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Pages 42-50"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000999/pdfft?md5=f74940c5a19df07f0411c52e62430bf0&pid=1-s2.0-S0923181124000999-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141322203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foxp3+ Treg control allergic skin inflammation by restricting IFN-γ-driven neutrophilic infiltration and NETosis","authors":"","doi":"10.1016/j.jdermsci.2024.05.002","DOIUrl":"10.1016/j.jdermsci.2024.05.002","url":null,"abstract":"<div><h3>Background</h3><p>Atopic dermatitis (AD), a chronic inflammatory skin disease with T cell activation as a key feature, in which Th2 cell–mediated responses play a pivotal role. Regulatory T cells (Treg) are central immune cells that restrict autoimmunity and inflammation in the body. Patients with immune dysregulation, polyendocrinopathy, or enteropathy X-linked syndrome, an immune disease characterized by a deficiency in Treg, develop skin inflammation and allergic disorders, indicating that Treg play a crucial role in the development of allergic skin inflammation.</p></div><div><h3>Objective</h3><p>we investigated the underlying mechanisms by which Treg control cutaneous allergic inflammation.</p></div><div><h3>Methods</h3><p>An allergic skin inflammation mouse model was constructed using MC903, and Treg-depleted mouse model was constructed using diphtheria toxin. Neutralization of IFN-γ was constructed using anti-mouse-IFN-γ mouse antibody. Neutrophil infiltration was analyzed by flow cytometry and immunohistochemistry. Neutrophil extracellular traps (NETs), a process called NETosis, were detected using immunofluorescence. In vitro neutrophil stimulation and immunocytochemistry was conducted to demonstrate the effect of IFN-γ on NETosis.</p></div><div><h3>Results</h3><p>The depletion of Foxp3⁺ Treg led to significantly exacerbated AD-like skin inflammation, including increased recruitment of neutrophils and expression of Th1 cytokine IFN-γ. Neutrophil infiltrating in skin of Treg-depleted mice released more NETs than wild type. Neutralization of IFN-γ abolished neutrophil infiltration and NETosis in Treg-depleted mice. Neutrophils stimulated with IFN-γ were more prone to release NETs <em>in vitro</em>. Finally, Foxp3⁺ Treg control cutaneous allergic inflammation by regulating IFN-γ-driven neutrophilic infiltration and NETosis.</p></div><div><h3>Conclusion</h3><p>Our results highlight the previously underestimated Treg-IFN-γ-neutrophil inflammatory axis.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Pages 2-12"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141051237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editors Choice","authors":"","doi":"10.1016/S0923-1811(24)00142-7","DOIUrl":"10.1016/S0923-1811(24)00142-7","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Page 1"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124001427/pdfft?md5=a94b9248626e4e8dc7c177d4765c3723&pid=1-s2.0-S0923181124001427-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141630178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JSID2024-1","authors":"","doi":"10.1016/S0923-1811(24)00144-0","DOIUrl":"10.1016/S0923-1811(24)00144-0","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Page 51"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141630176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RAS-activated PI3K/AKT signaling sustains cellular senescence via P53/P21 axis in experimental models of psoriasis","authors":"","doi":"10.1016/j.jdermsci.2024.03.002","DOIUrl":"10.1016/j.jdermsci.2024.03.002","url":null,"abstract":"<div><h3>Background</h3><p>Psoriasis is a chronic immune-mediated skin disease in which upper epidermal keratinocytes exhibit a senescent-like phenotype. In psoriatic skin, a variety of inflammatory cytokines can activate intracellular pathways including phosphatidylinositol 3-kinase (PI3K)/AKT signaling and RAS effectors. AKT and RAS participate to cellular senescence, but currently their role in senescence responses occurring in psoriasis have not yet been investigated.</p></div><div><h3>Objective</h3><p>The role of AKT molecular axis and RAS activation was evaluated in the context of cellular senescence in psoriasis disease.</p></div><div><h3>Methods</h3><p>RAS/AKT involvement in senescence was analyzed in psoriatic keratinocytes cultures subjected to multiple passages to promote senescence <em>in vitro</em>, as well as in skin lesions of patients affected by psoriasis. The impact of pharmacological inhibition of PI3K/AKT pathway on senescence and inflammation responses was tested in senescent psoriatic keratinocytes and in a psoriasiform dermatitis murine model induced by RAS overexpression in the upper epidermis of mice.</p></div><div><h3>Results</h3><p>We found AKT hyperactivation associated to the upregulation of senescence markers, in senescent psoriatic keratinocyte cultures, as well as in skin lesions of psoriatic patients. AKT-induced senescence was sustained by constitutive RAS activation, and down-stream responses were mediated by P53/P21 axis. PI3K/AKT inhibition contrasted senescence processes induced by cytokines in psoriatic keratinocytes. Additionally, RAS-induced psoriasis-like dermatitis in mice was accompanied by AKT upregulation, increase of senescence marker expression and by skin inflammation. In this model, both senescence and inflammation were significantly reduced by selective AKT inhibition.</p></div><div><h3>Conclusion</h3><p>Therefore, targeting RAS-AKT pathway could be a promising novel strategy to counteract multiple psoriasis symptoms.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"115 1","pages":"Pages 21-32"},"PeriodicalIF":4.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0923181124000343/pdfft?md5=83c778d0d309fc983999cd4edf7b3056&pid=1-s2.0-S0923181124000343-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140271184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis of phenotypes and transcriptome characteristics reveal the best atopic dermatitis mouse model induced by MC903","authors":"Shan Zhang ,&nbsp;Xiaokai Fang ,&nbsp;Beilei Xu,&nbsp;Yuan Zhou,&nbsp;Fang Li,&nbsp;Yuwen Gao,&nbsp;Yang Luo,&nbsp;Xu Yao,&nbsp;Xiaochun Liu","doi":"10.1016/j.jdermsci.2024.05.003","DOIUrl":"10.1016/j.jdermsci.2024.05.003","url":null,"abstract":"<div><h3>Background</h3><p>Although several mouse models of exogenous-agent<strong>–</strong>induced atopic dermatitis (AD) are currently available, the lack of certainty regarding their similarity with human AD has limited their scientific value. Thus, comprehensive evaluation of the characteristics of mouse models and their similarity with human AD is essential.</p></div><div><h3>Objective</h3><p>To compare six different exogenous-agent<strong>–</strong>induced AD mouse models and find out the optimum models for study.</p></div><div><h3>Methods</h3><p>Female BALB/c mice underwent induction of AD-like dermatitis by MC903 alone or in combination with ovalbumin (OVA), dinitrofluorobenzene (DNFB) alone or in combination with OVA, OVA alone, or <em>Staphylococcus aureus</em>. Gross phenotype, total immunoglobulin E (IgE) level, histopathological manifestations, and skin lesion transcriptome were analyzed, and metagenomic sequencing of the gut microbiome was performed.</p></div><div><h3>Results</h3><p>The DNFB plus OVA model showed the highest disease severity, while the OVA model showed the lowest severity. The MC903 and MC903 plus OVA models showed high expression of T-helper (Th)2- and Th17-related genes; the DNFB and DNFB plus OVA models showed upregulation of Th1-, Th2-, and Th17-related genes; while the <em>S. aureus</em> inoculation model showed more enhanced Th1 and Th17 immune responses. In contrast to the other models, the OVA-induced model showed the lowest expression levels of inflammation-related genes, while the MC903 model shared the largest overlap with human AD profiles. The intestinal microbiota of all groups showed significant differences after modeling.</p></div><div><h3>Conclusion</h3><p>Each AD mouse model exhibited different characteristics. The MC903 model was the best to recapitulate most features of human AD among these exogenous-agent<strong>–</strong>induced AD models.</p></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 3","pages":"Pages 104-114"},"PeriodicalIF":4.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141145412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in activation of β-catenin in outer root sheath cells between the type of JAK inhibitor: An alternative mechanism promoting hair growth by JAK inhibitors in alopecia areata","authors":"Jung-Min Shin,&nbsp;Yeounkuk Sung,&nbsp;Dongkyun Hong,&nbsp;Kyung-Eun Jung,&nbsp;Young-Joon Seo,&nbsp;Chang-Deok Kim,&nbsp;Young Lee","doi":"10.1016/j.jdermsci.2024.04.005","DOIUrl":"10.1016/j.jdermsci.2024.04.005","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"114 3","pages":"Pages 148-150"},"PeriodicalIF":4.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140909564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}