Journal of dermatological science最新文献

英文中文

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 通过局部注射由人脂肪间充质基质细胞分化的角质细胞样细胞，从组织学和分子学上恢复隐性萎缩性表皮松解症小鼠皮肤的 VII 型胶原蛋白。

IF 4.6

Journal of dermatological science

Pub Date : 2024-07-01 DOI: 10.1016/j.jdermsci.2024.05.004

Background

Recessive dystrophic epidermolysis bullosa (RDEB) is a severe skin fragility disorder caused by mutations in the COL7A1 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.

Objective

We investigated whether KC-AD-MSCs transplantation ameliorated the RDEB phenotype severity in the grafted skin of a RDEB mouse model (col7a1-null) on the back of the immunodeficient mouse.

Methods

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.

Results

Neodeposition of COL7 and generation of anchoring fibrils at the dermal-epidermal junction were observed, although experiments were based on qualitative.

Conclusion

KC-AD-MSCs may correct the COL7 insufficiency, repair defective/reduced anchoring fibrils, and improve skin integrity in RDEB patients.

背景：隐性萎缩性表皮松解症（RDEB）是一种严重的皮肤脆性疾病，由 COL7A1 基因突变引起，该基因编码 VII 型胶原蛋白（COL7），而 VII 型胶原蛋白是表皮与真皮之间锚定纤维的主要成分。RDEB 患者的皮肤持续糜烂经常导致顽固性溃疡。脂肪间充质干细胞（AD-MSCs）易于大量采集，且免疫原性低。因此，它们适合临床使用，包括涉及异体细胞移植的应用。与未分化的 AD-MSCs 相比，由 AD-MSCs 转分化而来的角质细胞样细胞（KC-AD-MSCs）表达更多的 COL7，可促进皮肤伤口愈合，减少挛缩。因此，这些细胞可用于治疗 RDEB 患者的皮肤溃疡：我们研究了移植 KC-AD-MSCs 是否能改善 RDEB 小鼠模型（col7a1-null）免疫缺陷小鼠背部移植皮肤的 RDEB 表型严重程度：方法：将 KC-AD-MSCs 皮内注射到皮肤移植周围区域，7 天后重复这一过程。间隔 7 天后，收获植皮：结论：KC-AD-间充质干细胞可修复皮肤损伤：结论：KC-AD-间充质干细胞可纠正 RDEB 患者的 COL7 缺乏，修复缺损/减少的锚定纤维，改善皮肤完整性。

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引用次数: 0

Foxp3+ Treg control allergic skin inflammation by restricting IFN-γ-driven neutrophilic infiltration and NETosis Foxp3+ Treg通过限制IFN-γ驱动的中性粒细胞浸润和NETosis控制过敏性皮肤炎症

IF 4.6

Journal of dermatological science

Pub Date : 2024-07-01 DOI: 10.1016/j.jdermsci.2024.05.002

Background

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.

Objective

we investigated the underlying mechanisms by which Treg control cutaneous allergic inflammation.

Methods

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.

Results

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 in vitro. Finally, Foxp3⁺ Treg control cutaneous allergic inflammation by regulating IFN-γ-driven neutrophilic infiltration and NETosis.

Conclusion

Our results highlight the previously underestimated Treg-IFN-γ-neutrophil inflammatory axis.

背景特应性皮炎（AD）是一种以 T 细胞活化为主要特征的慢性炎症性皮肤病，其中 Th2 细胞介导的反应起着关键作用。调节性 T 细胞（Treg）是限制体内自身免疫和炎症的中枢免疫细胞。目的我们研究了Treg控制皮肤过敏性炎症的内在机制。方法用MC903构建过敏性皮肤炎症小鼠模型，用白喉毒素构建Treg耗竭小鼠模型。使用抗小鼠-IFN-γ小鼠抗体构建 IFN-γ 中和模型。中性粒细胞浸润通过流式细胞术和免疫组化进行分析。使用免疫荧光检测中性粒细胞胞外捕获物（NET），这一过程被称为NETosis。结果Foxp3+ Treg的耗竭导致AD样皮肤炎症明显加重，包括中性粒细胞招募增加和Th1细胞因子IFN-γ的表达。与野生型相比，Treg缺失小鼠皮肤中浸润的中性粒细胞释放出更多的NET。中和 IFN-γ 可消除 Treg 清除小鼠的中性粒细胞浸润和 NETosis。受到 IFN-γ 刺激的中性粒细胞更容易在体外释放 NET。最后，Foxp3+ Treg 通过调节 IFN-γ 驱动的中性粒细胞浸润和 NETosis 控制皮肤过敏炎症。

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引用次数: 0

Editors Choice 编辑推荐

IF 4.6

Journal of dermatological science

Pub Date : 2024-07-01 DOI: 10.1016/S0923-1811(24)00142-7

引用次数: 0

JSID2024-1 JSID2024-1

IF 4.6

Journal of dermatological science

Pub Date : 2024-07-01 DOI: 10.1016/S0923-1811(24)00144-0

引用次数: 0

RAS-activated PI3K/AKT signaling sustains cellular senescence via P53/P21 axis in experimental models of psoriasis 在银屑病实验模型中，RAS 激活的 PI3K/AKT 信号通过 P53/P21 轴维持细胞衰老

IF 4.6

Journal of dermatological science

Pub Date : 2024-07-01 DOI: 10.1016/j.jdermsci.2024.03.002

Background

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.

Objective

The role of AKT molecular axis and RAS activation was evaluated in the context of cellular senescence in psoriasis disease.

Methods

RAS/AKT involvement in senescence was analyzed in psoriatic keratinocytes cultures subjected to multiple passages to promote senescence in vitro, 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.

Results

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.

Conclusion

Therefore, targeting RAS-AKT pathway could be a promising novel strategy to counteract multiple psoriasis symptoms.

背景银屑病是一种慢性免疫介导的皮肤病，上表皮角质形成细胞表现出衰老样表型。在银屑病皮肤中，多种炎症细胞因子可激活细胞内通路，包括磷脂酰肌醇 3- 激酶（PI3K）/AKT 信号转导和 RAS 效应因子。AKT和RAS参与了细胞衰老，但目前它们在银屑病衰老反应中的作用尚未得到研究。方法分析了AKT分子轴和RAS激活在银屑病细胞衰老中的作用。在衰老的银屑病角朊细胞和小鼠上表皮 RAS 过表达诱导的银屑病皮炎小鼠模型中测试了药理抑制 PI3K/AKT 通路对衰老和炎症反应的影响。AKT 诱导的衰老是由组成型 RAS 激活维持的，而下行反应则是由 P53/P21 轴介导的。PI3K/AKT 抑制与银屑病角质形成细胞因子诱导的衰老过程形成对比。此外，RAS 诱导的小鼠银屑病样皮炎伴随着 AKT 上调、衰老标志物表达增加和皮肤炎症。结论因此，靶向 RAS-AKT 通路可能是应对多种银屑病症状的一种很有前景的新策略。

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引用次数: 0

Comprehensive analysis of phenotypes and transcriptome characteristics reveal the best atopic dermatitis mouse model induced by MC903 表型和转录组特征的综合分析揭示了 MC903 诱导的最佳特应性皮炎小鼠模型

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.05.003

Shan Zhang , Xiaokai Fang , Beilei Xu, Yuan Zhou, Fang Li, Yuwen Gao, Yang Luo, Xu Yao, Xiaochun Liu

Background

Although several mouse models of exogenous-agent–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.

Objective

To compare six different exogenous-agent–induced AD mouse models and find out the optimum models for study.

Methods

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 Staphylococcus aureus. Gross phenotype, total immunoglobulin E (IgE) level, histopathological manifestations, and skin lesion transcriptome were analyzed, and metagenomic sequencing of the gut microbiome was performed.

Results

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 S. aureus 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.

Conclusion

Each AD mouse model exhibited different characteristics. The MC903 model was the best to recapitulate most features of human AD among these exogenous-agent–induced AD models.

背景尽管目前已有几种外源性激动剂诱导的特应性皮炎（AD）小鼠模型，但它们与人类特应性皮炎的相似性还不确定，这限制了它们的科学价值。方法用 MC903 单独或与卵清蛋白（OVA）、二硝基氟苯（DNFB）单独或与 OVA、OVA 单独或与金黄色葡萄球菌联合诱导雌性 BALB/c 小鼠发生类似 AD 的皮炎。结果 DNFB加OVA模型的疾病严重程度最高，而OVA模型的疾病严重程度最低。MC903和MC903加OVA模型显示出T辅助（Th）2和Th17相关基因的高表达；DNFB和DNFB加OVA模型显示出Th1、Th2和Th17相关基因的上调；而金黄色葡萄球菌接种模型则显示出更强的Th1和Th17免疫反应。与其他模型相比，OVA诱导模型的炎症相关基因表达水平最低，而MC903模型与人类AD特征的重叠程度最高。结论每个AD小鼠模型都表现出不同的特征。结论每种AD小鼠模型都表现出不同的特征，MC903模型是这些外源性试剂诱导的AD模型中最能再现人类AD特征的模型。

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引用次数: 0

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 不同类型的 JAK 抑制剂在外根鞘细胞中激活β-catenin 的差异：JAK抑制剂促进脱发症患者毛发生长的另一种机制。

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.04.005

Jung-Min Shin, Yeounkuk Sung, Dongkyun Hong, Kyung-Eun Jung, Young-Joon Seo, Chang-Deok Kim, Young Lee

引用次数: 0

JSID2024-1 JSID2024-1

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/S0923-1811(24)00122-1

引用次数: 0

Metabolome analyses of skin dialysate: Insights into skin interstitial fluid biomarkers 皮肤透析液的代谢组分析：皮肤间质液生物标志物透视。

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.04.001

Akihiko Oharazawa , Gulinu Maimaituxun , Koichi Watanabe , Takeshi Nishiyasu , Naoto Fujii

Background

Metabolites in biofluids can serve as biomarkers for diagnosing diseases and monitoring body conditions. Among the available biofluids, interstitial fluid (ISF) in the skin has garnered considerable attention owing to its advantages, which include inability to clot, easy access to the skin, and possibility of incorporating wearable devices. However, the scientific understanding of skin ISF composition is limited.

Objective

In this study, we aimed to compare metabolites between skin dialysate containing metabolites from the skin ISF and venous blood (plasma) samples, both collected under resting states.

Methods

We collected forearm skin dialysate using intradermal microdialysis alongside venous blood (plasma) samples from 12 healthy young adults. We analyzed these samples using capillary electrophoresis–fourier transform mass spectrometry–based metabolomics (CE–FTMS).

Results

Significant positive correlations were observed in 39 metabolites between the skin dialysate and plasma, including creatine (a mitochondrial disease biomarker), 1-methyladenosine (an early detection of cancer biomarker), and trimethylamine N-oxide (a posterior predictor of heart failure biomarker). Based on the Human Metabolome Technologies database, we identified 12 metabolites unique to forearm skin dialysate including nucleic acids, benzoate acids, fatty acids, amino acids, ascorbic acid, 3-methoxy-4-hydroxyphenylethyleneglycol (an Alzheimer’s disease biomarker), and cysteic acid (an acute myocardial infarction biomarker).

Conclusion

We show that some venous blood biomarkers may be predicted from skin dialysate or skin ISF, and that these fluids may serve as diagnostic and monitoring tools for health and clinical conditions.

背景：生物流体中的代谢物可作为诊断疾病和监测身体状况的生物标志物。在现有的生物流体中，皮肤间质液（ISF）因其不易凝结、易于接触皮肤以及可纳入可穿戴设备等优点而备受关注。然而，科学界对皮肤 ISF 成分的了解还很有限：在这项研究中，我们旨在比较含有皮肤 ISF 代谢物的皮肤透析液与静脉血（血浆）样本之间的代谢物：我们使用皮内微透析法采集了 12 名健康年轻人的前臂皮肤透析液和静脉血液（血浆）样本。我们使用毛细管电泳-傅立叶变换质谱法（CE-FTMS）对这些样本进行了代谢组学分析：结果：在皮肤透析液和血浆之间的 39 种代谢物中观察到了显著的正相关性，包括肌酸（线粒体疾病生物标志物）、1-甲基腺苷（癌症早期检测生物标志物）和三甲胺 N-氧化物（心力衰竭后期预测生物标志物）。根据人类代谢组技术数据库，我们确定了 12 种前臂皮肤透析液特有的代谢物，包括核酸、苯甲酸、脂肪酸、氨基酸、抗坏血酸、3-甲氧基-4-羟基苯乙二醇（一种阿尔茨海默病生物标记物）和半胱氨酸（一种急性心肌梗死生物标记物）：我们的研究表明，一些静脉血生物标志物可以从皮肤透析液或皮肤ISF中预测出来，这些液体可以作为健康和临床状况的诊断和监测工具。

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引用次数: 0

Obituary: Thomas Fletcher Tedder, PhD (1956–2024) 讣告：Thomas Fletcher Tedder 博士（1956-2024 年）。

IF 4.6

Journal of dermatological science

Pub Date : 2024-06-01 DOI: 10.1016/j.jdermsci.2024.04.003

Minoru Hasegawa , Manabu Fujimoto , Takafumi Kadono , Yasuhiro Fujisawa , Masahiro Kamata , Takashi Matsushita , Shinichi Sato

引用次数: 0

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