Journal of dermatological science最新文献

英文中文

RN7SL1 overexpression promotes cell proliferation in cutaneous T-cell lymphoma via miR-34a-5p/MYCN axis. RN7SL1 过表达通过 miR-34a-5p/MYCN 轴促进皮肤 T 细胞淋巴瘤的细胞增殖。

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-20 DOI: 10.1016/j.jdermsci.2025.03.003

Tingting Li, Jiachen Sun, Guanyu Wang, Yimeng Wang, Chunlei Zhang

Background: Cutaneous T-cell lymphoma (CTCL) is a type of lymphoma that presents in skin tissue without evidence of extracutaneous disease. Emerging evidence indicates that long noncoding RNA-RN7SL1 serves as crucial effectors in modulating progression of different malignancies, including breast cancer, liver cancer, and other neoplasms.

Objective: To figure out the role of RN7SL1 in the pathogenesis of CTCL.

Methods: We detected RN7SL1 expression of CTCL patients by quantitative real-time polymerase chain reaction and fluorescent in situ hybridization. CTCL cell lines were transfected with lentiviral-based RN7SL1 gene knockdown vectors. Whole transcriptome sequencing was conducted to investigate differentially expressed miRNA and mRNA in CTCL, and we used qRT-PCR, RNA immunoprecipitation, dual-luciferase assay, RNA pull down and Western Blotting to further detect the relation of miRNA and mRNA. Also, we have verified above results in mice and clinical samples.

Results: LncRNA-RN7SL1 was overexpressed in CTCL compared with benign inflammatory dermatosis and was related to the TNMB stage of mycosis fungoides and Sézary syndrome (higher expression in IIB-IVB stage than IA-IIA stage). Additionally, the proliferation of CTCL cell lines HH and Hut78 was weakened, but apoptosis was facilitated by RN7SL1 downregulation, resulting in a reduced tumorigenic capacity in vivo. Subsequently, Whole transcriptome sequencing and target validation indicated that the RN7SL1/miR-34a-5p/MYCN axis may promoted malignant behavior in CTCL.

Conclusion: Our study suggested that RN7SL1 promoted malignant behavior by targeting miR-34a-5p/MYCN signaling. This finding might facilitate the discovery of novel biomarkers for CTCL diagnosis and treatment.

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引用次数: 0

Immune signatures across different stages of cutaneous squamous cell carcinoma.

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-20 DOI: 10.1016/j.jdermsci.2025.03.002

Laure Favot-Laforge, Elodie Muzotte, Walid Mahfouf, Jerome Rambert, Muriel Cario, François Moisan, Lea Dousset, Hamid-Reza Rezvani

引用次数: 0

Genetics and epigenetics in vitiligo

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2025.01.004

Ken Okamura, Tamio Suzuki

Vitiligo, a complex autoimmune disorder characterized by melanocyte destruction, arises from an intricate interplay of genetic, epigenetic, immune, and environmental factors. Genome-wide association studies (GWAS) have identified over 50 susceptibility loci, including key genes within the MHC region and those involved in immunity, oxidative stress, and melanogenesis. Concurrently, epigenetic research has unraveled regulatory networks critical to vitiligo pathogenesis, with a focus on DNA methylation and non-coding RNAs (e.g., microRNAs, long non-coding RNAs, and circular RNAs). These advancements provide deeper insights into gene regulation, immune processes, and cellular dynamics. This review integrates findings from genetic and epigenetic studies to offer a comprehensive understanding of molecular mechanisms of vitiligo, paving the way for innovative, personalized therapeutic approaches.

引用次数: 0

Cytosolic mtDNA-cGAS-STING axis mediates melanocytes pyroptosis to promote CD8+ T-cell activation in vitiligo 细胞质mtDNA-cGAS-STING轴介导黑色素细胞热解，促进白癜风患者CD8+T细胞的活化。

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2024.12.002

Xinya Xu , Xinhua Lu , Yue Zheng , Yang Xie , Wei Lai

Background

The cGAS-STING axis, a DNA sensor pathway, has recently emerged as a key hub in sensing stress signals and initiating the immune cascade in several diseases. However, its role in the pathogenesis of vitiligo remains unclear.

Objective

To explore the pathogenic role of the cGAS-STING axis in linking oxidative stress and CD8⁺ T-cell-mediated anti-melanocytic immunity in vitiligo.

Methods

The expression status of the cGAS-STING axis and cytosolic mtDNA were evaluated in the oxidatively stressed epidermal cells and vitiligo perilesional skin, respectively. Then, we investigated the activation of cGAS-STING axis in mtDNA-treated melanocytes, and the influence of cGAS or STING silencing on mtDNA-induced melanocytes pyroptosis. Finally, the paracrine effects of melanocytes pyroptosis on CD8⁺ T cell activation were explored.

Results

We initially demonstrated that the cGAS-STING axis in melanocytes was highly susceptible to oxidative stress and activated in the vitiliginous melanocytes of perilesional skin, accompanied by enhanced cytosolic mtDNA accumulation. Our mechanistic in vitro experiments confirmed that oxidative stress-induced mitochondrial damage in epidermal cells led to cytosolic mtDNA accumulation, which served as a trigger in activating the cGAS-STING axis in melanocytes. Furthermore, the cytosolic mtDNA-cGAS-STING axis was verified to mediate melanocytes pyroptosis. More importantly, we found that IL-1β and IL-18 produced by pyroptotic melanocytes promoted the activation of CD8⁺ T cells from patients with vitiligo.

Conclusion

The present study confirmed that the cytosolic mtDNA-cGAS-STING axis of melanocytes played an important role in oxidative stress-triggered CD8⁺ T-cell response, providing novel insights into mechanisms underlying vitiligo onset.

背景：cGAS-STING轴是一种DNA传感器通路，最近已成为在多种疾病中感知应激信号和启动免疫级联的关键枢纽。然而，它在白癜风发病机制中的作用仍不清楚：探讨cGAS-STING轴在白癜风患者氧化应激和CD8+ T细胞介导的抗黑色素细胞免疫中的致病作用：方法：分别评估了氧化应激表皮细胞和白癜风周围皮肤中cGAS-STING轴和细胞膜mtDNA的表达状况。然后，我们研究了经mtDNA处理的黑色素细胞中cGAS-STING轴的激活情况，以及cGAS或STING沉默对mtDNA诱导的黑色素细胞脓毒症的影响。最后，我们还探讨了黑色素细胞热凋亡对 CD8+ T 细胞活化的旁分泌效应：我们初步证明了黑色素细胞中的 cGAS-STING 轴极易受到氧化应激的影响，并在绒毛周围皮肤的白癜风黑色素细胞中被激活，同时伴随着细胞膜 mtDNA 积累的增强。我们的体外机理实验证实，氧化应激诱导的表皮细胞线粒体损伤会导致细胞膜mtDNA积累，而mtDNA积累是激活黑色素细胞cGAS-STING轴的触发器。此外，我们还验证了细胞膜 mtDNA-cGAS-STING 轴介导了黑色素细胞的脓毒症。更重要的是，我们发现嗜热黑色素细胞产生的IL-1β和IL-18能促进白癜风患者CD8+T细胞的活化：本研究证实，黑色素细胞的细胞质mtDNA-cGAS-STING轴在氧化应激触发的CD8+ T细胞反应中发挥了重要作用，为了解白癜风的发病机制提供了新的视角。

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引用次数: 0

Unveiling intratumoral heterogeneity in high-risk cutaneous squamous cell carcinoma using single-cell spatial enhanced resolution omics-sequencing (Stereo-seq) 利用单细胞空间增强分辨率组学测序（Stereo-seq）揭示高风险皮肤鳞状细胞癌的肿瘤内异质性。

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2024.11.001

Jesse Veenstra , Ian Loveless , Peter Dimitrion , Indra Adrianto , David Ozog , Qing-Sheng Mi

引用次数: 0

Type 2 cytokine-JAK1 signaling is involved in the development of dry skin-induced mechanical alloknesis 2型细胞因子- jak1信号通路参与干性皮肤机械异位的发生。

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2024.10.002

Yui Toyosawa , Eriko Komiya , Takahide Kaneko , Yasushi Suga , Mitsutoshi Tominaga , Kenji Takamori

Background

Mechanical alloknesis (m-alloknesis) is itch hypersensitivity induced by normally innocuous stimuli. It is sometimes observed in dry skin based itch-related diseases such as atopic dermatitis (AD), and often triggers the vicious itch-scratch cycle. The acetone-ether and water (AEW) mouse model mimics dry skin-induced m-alloknesis, yet its underlying mechanism remains unclear. Janus kinase (JAK) inhibitors are used to treat AD, but their effects on m-alloknesis are not fully known.

Objective

To reveal the effects of various oral JAK inhibitors on m-alloknesis and their action points, using AEW model.

Methods

AEW model was prepared by treatment with a mixture of acetone-ether, and they were orally administrated a JAK1/2 inhibitor baricitinib, a selective JAK1 inhibitor abrocitinib, or a JAK2 selective inhibitor AZ960, and evaluated m-alloknesis score as the total number of scratching responses in 30 mechanical stimulations. To further elucidate the mechanism of action, IL-4, IL-13 or thymic stromal lymphopoietin (TSLP) or their neutralizing antibodies were also applied to mice. In addition, the levels of these cytokines in mouse skin were measured using multiple immunoassays.

Results

All of JAK inhibitors effectively reduced m-alloknesis, with abrocitinib demonstrating the most significant inhibition. The neutralizing antibodies against IL-4, IL-13, and TSLP inhibited m-alloknesis in AEW mice. Intradermal administration of IL-4, IL-13, or TSLP induced m-alloknesis, and abrocitinib effectively mitigated each cytokine-induced response. Highly sensitive assays detected IL-4, IL-13, IL-31 and TSLP in AEW-treated skin, with TSLP levels significantly increased.

Conclusion

Type 2 cytokine-JAK1 signaling is involved in the development of m-alloknesis in dry skin.

背景：机械异位是由通常无害的刺激引起的瘙痒过敏。它有时见于皮肤干燥性瘙痒相关疾病，如特应性皮炎（AD），并经常引发恶性瘙痒-抓伤循环。丙酮醚和水（AEW）小鼠模型模拟干皮肤诱导的m-异变，但其潜在机制尚不清楚。Janus kinase （JAK）抑制剂用于治疗AD，但其对m- allokesis的影响尚不完全清楚。目的：采用AEW模型，观察各种口服JAK抑制剂对m-异位化及其作用点的影响。方法：采用丙酮醚混合物治疗AEW模型，分别口服JAK1/2抑制剂baricitinib、JAK1选择性抑制剂abrocitinib或JAK2选择性抑制剂AZ960，并以30次机械刺激下挠性反应的总次数作为m-alloknesis评分。为了进一步阐明其作用机制，还将IL-4、IL-13或胸腺基质淋巴生成素（TSLP）或其中和抗体应用于小鼠。此外，这些细胞因子的水平在小鼠皮肤测量使用多种免疫分析。结果：所有JAK抑制剂均能有效降低m-异变，其中阿布替尼的抑制作用最显著。抗IL-4、IL-13和TSLP的中和抗体抑制AEW小鼠的m-异变。皮内给予IL-4、IL-13或TSLP诱导的m-异位，以及阿布昔替尼有效地减轻了每种细胞因子诱导的反应。高灵敏度检测方法检测了aew处理皮肤中IL-4、IL-13、IL-31和TSLP， TSLP水平显著升高。结论：2型细胞因子- jak1信号通路参与干性皮肤m-异位的发生。

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引用次数: 0

Melatonin mitigates UV-induced tumorigenesis and suppresses hearing function deterioration in Xpa-deficient mice

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2025.01.003

Mariko Tsujimoto , Takeshi Fujita , Tatsuya Furukawa , Yaeno Arima , Ken-Ichi Nibu , Chikako Nishigori

Background

Xeroderma pigmentosum (XP) is caused by impaired DNA repair of UV-induced dipyrimidine-photoproducts. XP cells also show impaired repair/removal of ROS or oxidative DNA lesions caused by UV or 4-nitroquinolline 1-oxide (4NQO). Gene profiling indicated that inflammatory response-related genes are significantly upregulated after UV exposure in XP-A model mice.

Objective

Since XP cells are in the state of oxidative stress and inflammation, we aimed to search for therapeutic agents from anti-oxidants/anti-inflammatory drugs, that potentially improve XP symptoms.

Methods

Several antioxidants were examined for reducing 4NQO-induced oxidative cytotoxicity or UV-induced oxidative DNA damage in XP-A cells. Among them, we focused on melatonin and evaluated its improving effect for Xpa-deficient MEF on UV-induced cytotoxicity and ROS production, and for Xpa-deficient mice on UV-induced skin tumorigenesis and auditory brainstem responses as one of the neurological symptoms.

Results

Melatonin and nicotinamide attenuated 4NQO-induced oxidative cytotoxicity. UV-induced intracellular ROS production and cytotoxicity were improved by melatonin for Xpa-deficient MEF. Finally, the administration of melatonin mitigated UV-induced skin inflammation and tumorigenesis and suppressed hearing deterioration in Xpa-deficient mice.

Conclusion

Our results show that melatonin could alleviate XP symptoms through its anti-inflammatory and antioxidant properties.

{"title":"Melatonin mitigates UV-induced tumorigenesis and suppresses hearing function deterioration in Xpa-deficient mice","authors":"Mariko Tsujimoto , Takeshi Fujita , Tatsuya Furukawa , Yaeno Arima , Ken-Ichi Nibu , Chikako Nishigori","doi":"10.1016/j.jdermsci.2025.01.003","DOIUrl":"10.1016/j.jdermsci.2025.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Xeroderma pigmentosum (XP) is caused by impaired DNA repair of UV-induced dipyrimidine-photoproducts. XP cells also show impaired repair/removal of ROS or oxidative DNA lesions caused by UV or 4-nitroquinolline 1-oxide (4NQO). Gene profiling indicated that inflammatory response-related genes are significantly upregulated after UV exposure in XP-A model mice.</div></div><div><h3>Objective</h3><div>Since XP cells are in the state of oxidative stress and inflammation, we aimed to search for therapeutic agents from anti-oxidants/anti-inflammatory drugs, that potentially improve XP symptoms.</div></div><div><h3>Methods</h3><div>Several antioxidants were examined for reducing 4NQO-induced oxidative cytotoxicity or UV-induced oxidative DNA damage in XP-A cells. Among them, we focused on melatonin and evaluated its improving effect for <em>Xpa</em>-deficient MEF on UV-induced cytotoxicity and ROS production, and for <em>Xpa-</em>deficient mice on UV-induced skin tumorigenesis and auditory brainstem responses as one of the neurological symptoms.</div></div><div><h3>Results</h3><div>Melatonin and nicotinamide attenuated 4NQO-induced oxidative cytotoxicity. UV-induced intracellular ROS production and cytotoxicity were improved by melatonin for <em>Xpa</em>-deficient MEF. Finally, the administration of melatonin mitigated UV-induced skin inflammation and tumorigenesis and suppressed hearing deterioration in <em>Xpa</em>-deficient mice.</div></div><div><h3>Conclusion</h3><div>Our results show that melatonin could alleviate XP symptoms through its anti-inflammatory and antioxidant properties.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 81-87"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076759","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}

引用次数: 0

Editor's choice

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/S0923-1811(25)00033-7

引用次数: 0

The role and mechanism of JAK2 inhibitor in endothelial mesenchymal transition in systemic sclerosis

IF 4.6

Journal of dermatological science

Pub Date : 2025-03-01 DOI: 10.1016/j.jdermsci.2025.02.001

Qingyan Luo , Xiaoheng Wang , Yanling Zhang , Wenrong Xie , Lina Liang , Yingping Xu , Yunshen Liang , Suyun Ji

Background

Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular endothelial dysfunction and damage, immune dysregulation and fibrosis. Endothelial mesenchymal transition (EndoMT) has been implicated in the skin fibrosis of SSc. Many studies have demonstrated that janus kinase type2 (JAK2) inhibitor can alleviate skin fibrosis in both SSc patients and bleomycin (BLM)-induced mouse models of SSc. However, the potential therapeutic effect of JAK2 inhibitor on EndoMT in SSc skin, along with the underlying molecular mechanisms, remains unexplored.

Objective

To investigate the effects of JAK2 inhibitor on the EndoMT in SSc skin and to elucidate the associated molecular mechanisms.

Methods

Wild-type female C57BL/6 mice were divided into several groups to assess the effects of JAK2 inhibitor on EndoMT through H&E staining, masson staining, immunofluorescence and single-cell RNA-sequencing (scRNA-seq). Cultured human umbilical vein endothelial cells (HUVECs) were used to explore the mechanism of action of JAK2 inhibitor on EndoMT using immunofluorescence, quantitative RT-PCR, RNA sequencing and western blot.

Results

JAK2 inhibition improved skin fibrosis, reduced CD31/α-SMA co-localisation and the number of EndoMT-activated vascular endothelial cells in bleomycin-induced SSc mice. Treatment of HUVECs with TGF-β or BLM led to a myofibroblast-like morphology and markers, along with downregulation of endothelial cell features, which were reversed following JAK2 inhibition. The activation of the PI3K/Akt/mTOR pathway was involved in EndoMT in HUVECs induced by TGF-β/BLM, and this activation was attenuated by JAK2 inhibition.

Conclusions

JAK2 inhibitor may serve as an effective treatment for EndoMT in SSc, potentially through modulation of the PI3K/Akt/mTOR signaling pathway.

{"title":"The role and mechanism of JAK2 inhibitor in endothelial mesenchymal transition in systemic sclerosis","authors":"Qingyan Luo , Xiaoheng Wang , Yanling Zhang , Wenrong Xie , Lina Liang , Yingping Xu , Yunshen Liang , Suyun Ji","doi":"10.1016/j.jdermsci.2025.02.001","DOIUrl":"10.1016/j.jdermsci.2025.02.001","url":null,"abstract":"<div><h3>Background</h3><div>Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular endothelial dysfunction and damage, immune dysregulation and fibrosis. Endothelial mesenchymal transition (EndoMT) has been implicated in the skin fibrosis of SSc. Many studies have demonstrated that janus kinase type2 (JAK2) inhibitor can alleviate skin fibrosis in both SSc patients and bleomycin (BLM)-induced mouse models of SSc. However, the potential therapeutic effect of JAK2 inhibitor on EndoMT in SSc skin, along with the underlying molecular mechanisms, remains unexplored.</div></div><div><h3>Objective</h3><div>To investigate the effects of JAK2 inhibitor on the EndoMT in SSc skin and to elucidate the associated molecular mechanisms.</div></div><div><h3>Methods</h3><div>Wild-type female C57BL/6 mice were divided into several groups to assess the effects of JAK2 inhibitor on EndoMT through H&E staining, masson staining, immunofluorescence and single-cell RNA-sequencing (scRNA-seq). Cultured human umbilical vein endothelial cells (HUVECs) were used to explore the mechanism of action of JAK2 inhibitor on EndoMT using immunofluorescence, quantitative RT-PCR, RNA sequencing and western blot.</div></div><div><h3>Results</h3><div>JAK2 inhibition improved skin fibrosis, reduced CD31/α-SMA co-localisation and the number of EndoMT-activated vascular endothelial cells in bleomycin-induced SSc mice. Treatment of HUVECs with TGF-β or BLM led to a myofibroblast-like morphology and markers, along with downregulation of endothelial cell features, which were reversed following JAK2 inhibition. The activation of the PI3K/Akt/mTOR pathway was involved in EndoMT in HUVECs induced by TGF-β/BLM, and this activation was attenuated by JAK2 inhibition.</div></div><div><h3>Conclusions</h3><div>JAK2 inhibitor may serve as an effective treatment for EndoMT in SSc, potentially through modulation of the PI3K/Akt/mTOR signaling pathway.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"117 3","pages":"Pages 71-80"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538268","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}

引用次数: 0

Triclosan exacerbates atopic dermatitis in mouse models via thymic stromal lymphopoietin.

IF 4.6

Journal of dermatological science

Pub Date : 2025-02-28 DOI: 10.1016/j.jdermsci.2025.02.007

Marie Charlotte Schuppe, Patryk Porebski, Katharina Klara Hahn, Kexin Liao, Anja Uhmann, Andrea Braun, Prasad Dasari, Michael Peter Schön, Timo Buhl

Background: Triclosan, a common antimicrobial agent, is widely used in personal-care products and as a topical antiseptic in atopic dermatitis (AD).

Objective: This study aimed to evaluate the topical and systemic effect of triclosan on AD in murine models, with a specific focus on the role of thymic stromal lymphopoietin (TSLP).

Methods: AD-like skin disease was induced by topical application of MC903 and house dust mites in female wildtype BALB/c, C57BL/6 J, and TSLP receptor (TSLPR)-knockout mouse strains. Mice were treated with triclosan both topically and systemically. Skin inflammation was assessed by measuring ear thickness. Infiltration of immune cells was analyzed by flow cytometry and immunohistochemistry (IHC). Cytokine expression was determined by quantitative real-time PCR.

Results: Triclosan application induced skin inflammation in a dose-dependent manner. Topical triclosan treatment increased ear inflammation and immune cell infiltration in AD-like mouse models. Systemic administration of triclosan also enhanced local AD-like skin reactions. Triclosan-induced skin inflammation was reduced in TSLP-receptor-knockout mice or by blocking TSLP, thus indicating the pivotal role of TSLP in mediating the immunological effects of triclosan.

Conclusions: Topical and systemic administration of triclosan exacerbates AD-like skin inflammation in murine models, with TSLP being a central mediator of this process. The translational relevance of these findings to human disease remains uncertain, as no direct human data are available.

{"title":"Triclosan exacerbates atopic dermatitis in mouse models via thymic stromal lymphopoietin.","authors":"Marie Charlotte Schuppe, Patryk Porebski, Katharina Klara Hahn, Kexin Liao, Anja Uhmann, Andrea Braun, Prasad Dasari, Michael Peter Schön, Timo Buhl","doi":"10.1016/j.jdermsci.2025.02.007","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2025.02.007","url":null,"abstract":"<p><strong>Background: </strong>Triclosan, a common antimicrobial agent, is widely used in personal-care products and as a topical antiseptic in atopic dermatitis (AD).</p><p><strong>Objective: </strong>This study aimed to evaluate the topical and systemic effect of triclosan on AD in murine models, with a specific focus on the role of thymic stromal lymphopoietin (TSLP).</p><p><strong>Methods: </strong>AD-like skin disease was induced by topical application of MC903 and house dust mites in female wildtype BALB/c, C57BL/6 J, and TSLP receptor (TSLPR)-knockout mouse strains. Mice were treated with triclosan both topically and systemically. Skin inflammation was assessed by measuring ear thickness. Infiltration of immune cells was analyzed by flow cytometry and immunohistochemistry (IHC). Cytokine expression was determined by quantitative real-time PCR.</p><p><strong>Results: </strong>Triclosan application induced skin inflammation in a dose-dependent manner. Topical triclosan treatment increased ear inflammation and immune cell infiltration in AD-like mouse models. Systemic administration of triclosan also enhanced local AD-like skin reactions. Triclosan-induced skin inflammation was reduced in TSLP-receptor-knockout mice or by blocking TSLP, thus indicating the pivotal role of TSLP in mediating the immunological effects of triclosan.</p><p><strong>Conclusions: </strong>Topical and systemic administration of triclosan exacerbates AD-like skin inflammation in murine models, with TSLP being a central mediator of this process. The translational relevance of these findings to human disease remains uncertain, as no direct human data are available.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588750","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}

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