Zinc oxide nanoparticles exacerbate skin epithelial cell damage by upregulating pro-inflammatory cytokines and exosome secretion in M1 macrophages following UVB irradiation-induced skin injury.

IF 7.2 1区 医学 Q1 TOXICOLOGY
Bour-Jr Wang, Yu-Ying Chen, Hui-Hsuan Chang, Rong-Jane Chen, Ying-Jan Wang, Yu-Hsuan Lee
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Abstract

Background: Zinc oxide nanoparticles (ZnONPs) are common materials used in skin-related cosmetics and sunscreen products due to their whitening and strong UV light absorption properties. Although the protective effects of ZnONPs against UV light in intact skin have been well demonstrated, the effects of using ZnONPs on damaged or sunburned skin are still unclear. In this study, we aimed to reveal the detailed underlying mechanisms related to keratinocytes and macrophages exposed to UVB and ZnONPs.

Results: We demonstrated that ZnONPs exacerbated mouse skin damage after UVB exposure, followed by increased transepidermal water loss (TEWL) levels, cell death and epithelial thickness. In addition, ZnONPs could penetrate through the damaged epithelium, gain access to the dermis cells, and lead to severe inflammation by activation of M1 macrophage. Mechanistic studies indicated that co-exposure of keratinocytes to UVB and ZnONPs lysosomal impairment and autophagy dysfunction, which increased cell exosome release. However, these exosomes could be taken up by macrophages, which accelerated M1 macrophage polarization. Furthermore, ZnONPs also induced a lasting inflammatory response in M1 macrophages and affected epithelial cell repair by regulating the autophagy-mediated NLRP3 inflammasome and macrophage exosome secretion.

Conclusions: Our findings propose a new concept for ZnONP-induced skin toxicity mechanisms and the safety issue of ZnONPs application on vulnerable skin. The process involved an interplay of lysosomal impairment, autophagy-mediated NLRP3 inflammasome and macrophage exosome secretion. The current finding is valuable for evaluating the effects of ZnONPs for cosmetics applications.

氧化锌纳米颗粒通过上调促炎细胞因子和外泌体分泌,加剧紫外线照射诱发的皮肤损伤后的皮肤上皮细胞损伤。
背景:氧化锌纳米粒子(ZnONPs)具有美白和强紫外线吸收特性,是皮肤相关化妆品和防晒产品中常用的材料。虽然 ZnONPs 对完整皮肤紫外线的保护作用已得到充分证实,但对受损或晒伤皮肤使用 ZnONPs 的效果仍不清楚。在这项研究中,我们旨在揭示与暴露于紫外线和 ZnONPs 的角质细胞和巨噬细胞有关的详细内在机制:结果:我们发现 ZnONPs 会加剧 UVB 暴露后小鼠皮肤的损伤,继而增加经表皮失水(TEWL)水平、细胞死亡和上皮厚度。此外,ZnONPs 还能穿透受损的上皮细胞,进入真皮层细胞,并通过激活 M1 巨噬细胞导致严重的炎症。机理研究表明,角质细胞同时暴露于紫外线和 ZnONPs 会导致溶酶体受损和自噬功能障碍,从而增加细胞外泌体的释放。然而,这些外泌体可被巨噬细胞吸收,从而加速了 M1 型巨噬细胞的极化。此外,ZnONPs还通过调节自噬介导的NLRP3炎性体和巨噬细胞外泌体的分泌,诱导M1巨噬细胞产生持久的炎症反应,并影响上皮细胞的修复:我们的研究结果为壬基酚诱导的皮肤毒性机制以及壬基酚应用于脆弱皮肤的安全性问题提出了一个新概念。这一过程涉及溶酶体损伤、自噬介导的 NLRP3 炎性体和巨噬细胞外泌体的相互作用。目前的发现对于评估 ZnONPs 在化妆品中的应用效果很有价值。
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来源期刊
CiteScore
15.90
自引率
4.00%
发文量
69
审稿时长
6 months
期刊介绍: Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.
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