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Effects of Particulate Matter in a Mouse Model of Oxazolone-Induced Atopic Dermatitis

机译:恶唑酮诱导的特应性皮炎小鼠模型中颗粒物质的影响

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Background: Recent epidemiological studies have demonstrated that air pollution is associated with the inflammatory response and may aggravate inflammatory skin diseases such as atopic dermatitis (AD). However, it is unclear whether particulate matter (PM) aggravates AD symptoms. Objective: The aim of this study was to investigate whether PM exposure affects the skin barrier dysfunction and aggravates AD symptoms using human keratinocytes (HaCaT) cells and a mouse model of oxazolone-induced AD-like skin. Methods: Standard reference material (SRM) 1649b, which mainly comprises polycyclic aromatic hydrocarbons, was used as the reference PM. HaCaT cells and mouse model of oxazolone-induced AD-like skin were treated with PM. The mRNA or protein expression levels of stratum corneum (SC) and tight junction (TJ) proteins, inflammatory cytokines, as well as clinical and histological changes of the AD-like skin of mouse model were evaluated. The expression of genes and proteins was analyzed by real-time polymerase chain reaction and Western blotting. Levels of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Results: The results revealed that PM downregulates the expression levels of several SC and TJ-related proteins in the mouse model with AD-like skin. Clinically, epidermal and dermal thickness was significantly increased and dermal inflammation was prominent in PM treated AD-like skin. Conclusion: In conclusion, we found that PM aggravates skin barrier dysfunction, clinically augmenting epidermal and dermal thickening with dermal inflammation in AD-like skin. These results suggest that PM may trigger the exacerbation of AD symptoms via skin barrier dysfunction-related mechanisms.
机译:背景:最近的流行病学研究表明,空气污染与炎症反应有关,可能加剧炎症皮肤病如特应性皮炎(AD)。然而,目前尚不清楚颗粒物质(PM)是否加剧了广告症状。目的:本研究的目的是调查PM暴露是否会影响皮肤屏障功能障碍,并使用人角蛋白细胞(HACAT)细胞和恶唑酮诱导的AD样皮肤的小鼠模型加剧AD症状。方法:主要包括多环芳烃(SRM)1649B,用作参考PM。 HACAT细胞和恶唑酮诱导的AD样皮肤的小鼠模型用PM处理。评估了角质层(SC)和紧密结(TJ)蛋白,炎症细胞因子以及小鼠模型的临床和临床和组织学改变的mRNA或蛋白表达水平。通过实时聚合酶链反应和蛋白质印迹分析基因和蛋白质的表达。通过酶联免疫吸附测定测量炎症细胞因子的水平。结果:结果表明,PM在小鼠模型中下调了几种SC和TJ相关蛋白的表达水平,用Ad样皮肤。临床上,表皮和皮肤厚度显着增加,PM处理的AD样皮肤中皮肤炎症突出。结论:总之,我们发现PM加剧皮肤屏障功能障碍,临床增强表皮和皮肤增厚,在ad样皮肤中具有皮肤炎症。这些结果表明PM可能通过皮肤屏障功能障碍相关机制触发AD症状的恶化。

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