三氯生通过胸腺基质淋巴生成素加重小鼠模型中的特应性皮炎。

IF 4.6
Marie Charlotte Schuppe , Patryk Porebski , Katharina Klara Hahn , Kexin Liao , Anja Uhmann , Andrea Braun , Prasad Dasari , Michael Peter Schön , Timo Buhl
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引用次数: 0

摘要

背景:三氯生是一种常见的抗菌药物,广泛应用于个人护理产品和特应性皮炎(AD)的局部抗菌剂。目的:本研究旨在评估三氯生对小鼠AD模型的局部和全身作用,特别关注胸腺基质淋巴生成素(TSLP)的作用。方法:对BALB/c、C57BL/6 J和TSLP受体(TSLPR)敲除的雌性野生型小鼠,局部应用MC903和室内尘螨诱导ad样皮肤病。小鼠局部和全身给予三氯生治疗。通过测量耳部厚度来评估皮肤炎症。采用流式细胞术和免疫组织化学(IHC)分析免疫细胞浸润情况。实时荧光定量PCR检测细胞因子表达。结果:应用三氯生诱导皮肤炎症呈剂量依赖性。局部三氯生治疗增加ad样小鼠模型的耳部炎症和免疫细胞浸润。全身给药三氯生也增强了局部ad样皮肤反应。TSLP受体敲除小鼠或通过阻断TSLP可减轻三氯生诱导的皮肤炎症,从而提示TSLP在介导三氯生免疫作用中的关键作用。结论:局部和全身给药三氯生加剧了小鼠模型ad样皮肤炎症,TSLP是这一过程的中心介质。这些发现与人类疾病的转化相关性仍然不确定,因为没有直接的人类数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Triclosan exacerbates atopic dermatitis in mouse models via thymic stromal lymphopoietin

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.
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