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Correlating Topographic Imaging and Raman Microscopy to Investigate Wound Re-Epithelialization. 将地形图成像和雷曼显微镜相关联,以研究伤口的再上皮化。
Pub Date : 2024-09-27 DOI: 10.1016/j.jid.2024.08.031
Pia Katharina Vestweber, Ines Ana Ederer, Ulrich Michael Rieger, Ernst H K Stelzer, Viktoria Planz, Maike Windbergs
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引用次数: 0
Profiling Long Noncoding RNA in Psoriatic Skin Using Single-Cell RNA Sequencing. 利用 scRNA-seq 分析银屑病皮肤中的 lncRNA。
Pub Date : 2024-09-27 DOI: 10.1016/j.jid.2024.09.010
Rachael Bogle, Matthew T Patrick, Sutharzan Sreeskandarajan, Mehrnaz Gharaee-Kermani, Haihan Zhang, Qinmengge Li, Ruiwen Zhou, Feiyang Ma, J Michelle Kahlenberg, Olesya Plazyo, James T Elder, Allison C Billi, Johann E Gudjonsson, Lam C Tsoi

The expressions of long noncoding RNAs (lncRNAs) and their roles in epidermal differentiation have been previously defined using bulk RNA sequencing. Despite their tissue-specific expression profiles, most lncRNAs are not well-annotated at the single-cell level. In this study, we evaluated the use of single-cell RNA sequencing to profile and characterize lncRNAs using data from 6 patients with psoriasis with paired uninvolved and lesional psoriatic skin. Despite their overall lower expression, we were able to detect >7000 skin-expressing lncRNAs and their cellular sources. Differential gene expression analysis revealed 137 differentially expressed lncRNAs in lesional psoriasis skin and identified 169 cell-type-specific lncRNAs. Keratinocytes had the highest number of differentially expressed lncRNA in psoriatic skin, which we validated using spatial transcriptomic data. We further showed that expression of the keratinocyte-specific lncRNA, AC020916.1, upregulated in lesional skin, is significantly correlated with expressions of genes participating in cell proliferation/epidermal differentiation, including SPRR2E and transcription factor ZFP36, particularly in the psoriatic skin. Our study highlights the potential for using single-cell RNA sequencing to profile skin-expressing lncRNA transcripts and to infer their cellular origins, providing a crucial approach that can be applied to the study of other inflammatory skin conditions.

以前曾利用批量 RNA-seq 确定了长非编码 RNA(lncRNA)的表达及其在表皮分化中的作用。尽管lncRNA具有组织特异性表达谱,但大多数lncRNA并没有在单细胞水平上得到很好的标注。在这里,我们使用来自 6 名银屑病患者的数据,评估了使用 scRNA-seq 对 lncRNAs 进行剖析和定性的情况。尽管它们的整体表达量较低,但我们还是检测到了超过 7,000 个皮肤表达的 lncRNA 及其细胞来源。差异基因表达分析揭示了银屑病(PP)皮损皮肤中137个差异表达的lncRNA,并确定了169个细胞类型特异的lncRNA。角质形成细胞在银屑病皮肤中差异表达的 lncRNA 数量最多,我们利用空间转录组数据验证了这一点。我们进一步发现,角质形成细胞特异性 lncRNA AC020916.1 的表达在病变皮肤中上调,与参与细胞增殖/表皮分化的基因(包括 SPRR2E 和转录因子 ZFP36)的表达显著相关,尤其是在银屑病皮肤中。我们的研究强调了利用 scRNA-seq 分析皮肤表达的 lncRNA 转录本并推断其细胞来源的潜力,提供了一种可用于研究其他炎症性皮肤病的重要方法。
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引用次数: 0
Evaluation of Benzene Presence and Formation in Benzoyl Peroxide Drug Products. 评估过氧化苯甲酰药物产品中苯的存在和形成。
Pub Date : 2024-09-27 DOI: 10.1016/j.jid.2024.09.009
Kaury Kucera, Nicola Zenzola, Amber Hudspeth, Mara Dubnicka, Wolfgang Hinz, Christopher G Bunick, Michael Girardi, Arash Dabestani, David Y Light

The potent carcinogen, benzene, is a known degradation product of benzoyl peroxide (BPO) and was recently reported to form when BPO drug products, used for acne and rosacea treatment, are incubated at body temperature and elevated temperatures expected during storage and transportation. This study provides evidence for a wide range of benzene concentrations (0.16 ppm to 35.30 ppm) detected by GC-MS in 111 over-the-counter BPO drug products tested and maintained at room temperature. A prescription encapsulated BPO drug product was stability tested at cold (2°C) and elevated temperature (50°C), resulting in no apparent benzene formation at 2°C, and high levels of benzene formation at 50°C, suggesting that encapsulation technology may not stabilize BPO drug products but cold storage may greatly reduce benzene formation. Face model experiments where BPO drug product was applied to PolyMethyl MethAcrylate (PMMA) photoprotection test skin plates and benzene was detected in surrounding air by SIFT-MS, showed detectable benzene through evaporation and substantial benzene formation when exposed to UV light at levels below peak sunlight. Results suggest that potential benzene exposure from formation during BPO drug product use poses significant risks independent of the starting benzene concentration.

苯是一种已知的过氧化苯甲酰(BPO)降解产物,最近有报告称,当用于治疗痤疮和红斑痤疮的 BPO 药物产品在体温以及储存和运输过程中的预期高温下孵育时,会产生苯。本研究提供的证据表明,在室温下测试和保存的 111 种非处方药 BPO 产品中,通过气相色谱-质谱仪检测到的苯浓度范围很广(0.16 ppm 至 35.30 ppm)。在低温(2°C)和高温(50°C)条件下对处方封装的 BPO 药物产品进行了稳定性测试,结果表明在 2°C 条件下没有明显的苯形成,而在 50°C 条件下苯的形成水平较高,这表明封装技术可能无法稳定 BPO 药物产品,但低温储存可能会大大减少苯的形成。在脸部模型实验中,将 BPO 药物产品涂抹在聚甲基丙烯酸甲酯(PMMA)光保护测试皮肤板上,并通过 SIFT-MS 检测周围空气中的苯,结果表明通过蒸发可检测到苯,当暴露在低于日照峰值水平的紫外线下时,会有大量苯形成。结果表明,在使用 BPO 药物产品的过程中,潜在的苯暴露会造成重大风险,与起始苯浓度无关。
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引用次数: 0
Molecular and Cellular Function of p63 in Skin Development and Genetic Diseases. p63 在皮肤发育和遗传疾病中的分子和细胞功能。
Pub Date : 2024-09-26 DOI: 10.1016/j.jid.2024.08.011
Daniela Di Girolamo, Enzo Di Iorio, Caterina Missero

The transcription factor p63 is a master regulator of multiple ectodermal derivatives. During epidermal commitment, p63 interacts with several chromatin remodeling complexes to transactivate epidermal-specific genes and repress transcription of simple epithelial and nonepithelial genes. In the postnatal epidermis, p63 is required to control the proliferative potential of progenitor cells, maintain epidermal integrity, and contribute to epidermal differentiation. Autosomal dominant sequence variant in p63 cause a spectrum of syndromic disorders that affect several tissues, including or derived from stratified epithelia. In this review, we describe the recent studies that have provided novel insights into disease pathogenesis and potential therapeutic targets.

转录因子 p63 是多种表皮衍生物的主调节因子。在表皮形成过程中,p63 与几种染色质重塑复合物相互作用,转激活表皮特异性基因,抑制简单上皮和非上皮基因的转录。在出生后的表皮中,p63 需要控制祖细胞的增殖潜能、维持表皮的完整性并促进表皮分化。p63 的常染色体显性序列变异会导致一系列综合症,影响多种组织,包括分层上皮或由分层上皮衍生的组织。在这篇综述中,我们将介绍最近的研究,这些研究为疾病的发病机制和潜在的治疗靶点提供了新的见解。
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引用次数: 0
Estimation of Body Mass Index from 3-Dimensional Total Body Photography. 通过三维全身摄影估算体重指数(BMI)。
Pub Date : 2024-09-26 DOI: 10.1016/j.jid.2024.06.1294
Sam Kahler, Brigid Betz-Stablein, Fabian Lee, Joachim Torrano, Monika Janda, Clare Primiero, H Peter Soyer, Dilki Jayasinghe
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引用次数: 0
Single-Cell RNA Sequencing Reveals Molecular Signatures that Distinguish Allergic from Irritant Contact Dermatitis. 单细胞 RNA 序列分析揭示了区分过敏性接触性皮炎和刺激性接触性皮炎的分子特征。
Pub Date : 2024-09-26 DOI: 10.1016/j.jid.2024.09.008
Michael L Frisoli, Wei-Che C Ko, Nuria Martinez, Khashayar Afshari, Yuqing Wang, Manuel Garber, John E Harris

Allergic contact dermatitis (ACD) is a pruritic skin disease caused by environmental chemicals that induce cell-mediated skin inflammation within susceptible individuals. Irritant contact dermatitis (ICD) is caused by direct damage to the skin barrier by environmental insults. Diagnosis can be challenging because both types of contact dermatitis can appear similar by visual examination, and histopathological analysis does not reliably distinguish ACD from ICD. To discover specific biomarkers of ACD and ICD, we characterized the transcriptomic and proteomic changes that occur within the skin during each type of contact dermatitis. We induced ACD and ICD in healthy human volunteers and sampled skin using a nonscarring suction blister biopsy method that collects interstitial fluid and cellular infiltrate. Single-cell RNA sequencing analysis revealed that cell-specific transcriptome differences rather than cell-type proportions best distinguished ACD from ICD. Allergy-specific genes were associated with upregulation of IFNG, and cell signaling network analysis implicated several other genes such as IL4, despite their low expression levels. We validated transcriptomic differences with proteomic assays on blister fluid and trained a logistic regression model on skin interstitial fluid proteins that could distinguish ACD from ICD and healthy control skin with 93% sensitivity and 93% specificity.

过敏性接触性皮炎(ACD)是一种瘙痒性皮肤病,由环境中的化学物质引起,诱发易感人群的细胞介导的皮肤炎症。刺激性接触性皮炎(ICD)是由环境刺激直接损伤皮肤屏障引起的。这两种类型的接触性皮炎在肉眼观察下可能相似,而组织病理学分析并不能可靠地区分刺激性接触性皮炎和刺激性接触性皮炎,因此诊断具有挑战性。为了发现 ACD 和 ICD 的特异性生物标志物,我们对每种类型的接触性皮炎期间皮肤内发生的转录组和蛋白质组变化进行了表征。我们在健康的人类志愿者身上诱发了 ACD 和 ICD,并使用非瘢痕吸疱活检法采集了皮肤样本,该方法可收集间质和细胞浸润。单细胞 RNA 序列分析显示,细胞特异性转录组差异而非细胞类型比例最能区分 ACD 和 ICD。过敏特异性基因与 IFNG 的上调有关,而细胞信号网络分析则牵涉到其他几个基因,如 IL4,尽管它们的表达水平较低。我们通过对水疱液的蛋白质组检测验证了转录组的差异,并对皮肤间质液蛋白质训练了一个逻辑回归模型,该模型能以 93% 的灵敏度和 93% 的特异性将 ACD 与 ICD 和健康对照皮肤区分开来。
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引用次数: 0
Significant Role of Autophagy in Melanosomal Degradation of Dermal Macrophages: Therapeutic Insight Regarding Hyperpigmentation with Uncertain Etiology. 自噬在真皮巨噬细胞黑质体降解中的重要作用--对病因不明的色素沉着症的治疗启示
Pub Date : 2024-09-25 DOI: 10.1016/j.jid.2024.09.007
Kisumi Takiguchi, Kazunori Yokoi, Daiki Murase, Masafumi Yokota, Keigo Kawabata, Yoshito Takahashi, Satoshi Minami, Shuhei Nakamura, Tamotsu Yoshimori, Rei Watanabe, Manabu Fujimoto, Atsushi Tanemura
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引用次数: 0
Mouse Models of Itch. 小鼠瘙痒模型
Pub Date : 2024-09-25 DOI: 10.1016/j.jid.2024.08.018
Daniel Yassky, Brian S Kim

Murine models are vital preclinical and biological tools for studying itch. In this paper, we explore how these models have enhanced our understanding of the mechanisms underlying itch through both acute and chronic itch models. We provide detailed protocols and recommend experimental setups for specific models to guide researchers in conducting itch research. We distinguish between what constitutes a bona fide pruritogen versus a stimulus that causes pruritogen release, an acute itch model versus a chronic itch model, and how murine models can capture aspects of pruritus in human disease. Finally, we highlight how mouse models of itch have transformed our understanding and development of therapeutics for chronic pruritus in patients.

小鼠模型是研究痒的重要临床前和生物学工具。在本文中,我们将探讨这些模型如何通过急性和慢性痒模型加深我们对痒的机制的了解。我们提供了详细的实验方案,并推荐了特定模型的实验设置,以指导研究人员开展痒研究。我们区分了什么是真正的瘙痒原,什么是导致瘙痒原释放的刺激,什么是急性瘙痒模型,什么是慢性瘙痒模型,以及小鼠模型如何捕捉人类疾病中瘙痒的各个方面。最后,我们强调了小鼠瘙痒模型如何改变了我们对患者慢性瘙痒症的理解和治疗方法的开发。
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引用次数: 0
Type XVII Collagen-Specific CD4+ T Cells Induce Bullous Pemphigoid by Producing IL-5. XVII型胶原蛋白特异性CD4+T细胞通过产生IL-5诱导大疱性类天疱疮。
Pub Date : 2024-09-24 DOI: 10.1016/j.jid.2024.08.026
Norihiro Yoshimoto, Ken Muramastsu, Takamasa Ito, Miao Zheng, Kentaro Izumi, Ken Natsuga, Hiroaki Iwata, Yoshinori Hasegawa, Hideyuki Ujiie

Bullous pemphigoid is an autoimmune subepidermal blistering disease caused by anti-type XVII collagen (COL17) antibodies. Bullous pemphigoid has some immunological features such as eosinophilic infiltration and the deposition of IgE autoantibodies in the skin; however, the mechanism behind such features remains largely unclear. We focused on the autoantigen-specific CD4+ T cells, which are considered to regulate immune response. We established COL17-specific CD4+ T cell lines in vitro. Wild-type mice were immunized with synthesized peptides that include a pathogenic epitope of COL17, and lymphocytes were subjected to a limiting dilution assay. We established 5 T cell lines and examined the pathogenicity by transferring them with COL17-primed B cells into Rag-2-/-/COL17-humanized mice that express human COL17 but not mouse COL17 in the skin. Notably, 3 lines induced bullous pemphigoid-like skin changes associated with subepidermal separation and eosinophilic infiltration histologically and the production of anti-COL17 antibodies. The other 2 lines did not induce such phenotypes. RNA-sequencing analysis revealed that T helper 2 cytokines, particularly IL-5, were highly expressed in the pathogenic T-cell lines. Anti-IL-5 antibody administration significantly reduced the skin changes and attenuated the production of autoantibodies. Thus, the production of IL-5 is critical for COL17-specific CD4+ T cells to induce bullous pemphigoid phenotypes in vivo.

大疱性类天疱疮(BP)是一种由抗十七型胶原(COL17)抗体引起的自身免疫性表皮下大疱性疾病。大疱性类天疱疮具有一些免疫学特征,如嗜酸性粒细胞浸润和 IgE 自身抗体在皮肤中沉积;然而,这些特征背后的机制在很大程度上仍不清楚。我们重点研究了被认为能调节免疫反应的自身抗原特异性 CD4+ T 细胞。我们在体外建立了 COL17 特异性 CD4+ T 细胞系。用包含 COL17 致病表位的合成肽免疫野生型小鼠,并对淋巴细胞进行限制稀释试验。我们建立了 5 个 T 细胞系,并将它们与 COL17 诱导的 B 细胞一起转移到皮肤中表达人 COL17 而非小鼠 COL17 的 Rag-2-/-/COL17 人源化小鼠体内,以检测其致病性。值得注意的是,有 3 个品系诱发了与表皮下分离和嗜酸性粒细胞浸润有关的 BP 样皮肤变化,并产生了抗 COL17 抗体。另外 2 个品系没有诱发此类表型。RNA 序列分析表明,Th2 细胞因子,尤其是 IL-5 在致病 T 细胞系中高度表达。服用抗 IL-5 抗体可明显减轻皮肤变化,并减少自身抗体的产生。因此,IL-5的产生对COL17特异性CD4+ T细胞在体内诱导BP表型至关重要。
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引用次数: 0
Hidradenitis Suppurativa Tunnels Invasive Transcriptional Signature. 化脓性扁桃体炎隧道侵袭转录特征
Pub Date : 2024-09-24 DOI: 10.1016/j.jid.2024.04.037
Stephan M Caucheteux, Vincent Piguet
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引用次数: 0
期刊
The Journal of investigative dermatology
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