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

被引:13
|
作者
Bae, Yoo Jung [1 ]
Park, Kui Young [1 ]
Han, Hye Sung [1 ]
Kim, Young Shin [2 ]
Hong, Ji Yeon [3 ]
Han, Tae Young [2 ]
Seo, Seong Jun [1 ]
机构
[1] Chung Ang Univ, Dept Dermatol, Coll Med, 102 Heukseok Ro, Seoul 06973, South Korea
[2] Eulji Univ, Nowon Eulji Med Ctr, Dept Dermatol, 68 Hangeulbiseok Ro, Seoul 01830, South Korea
[3] Seoul Natl Univ Hosp, Dept Dermatol, Seoul, South Korea
基金
新加坡国家研究基金会;
关键词
Air pollution; Atopic dermatitis; Epidermis; Particulate matter; SKIN BARRIER FUNCTION; AIR-POLLUTION; CARDIOVASCULAR-DISEASE; TERM EXPOSURE; DIFFERENTIATION; DYSFUNCTION; EXPRESSION; POLLUTANTS; PARTICLES; CYTOKINES;
D O I
10.5021/ad.2020.32.6.496
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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.
引用
收藏
页码:496 / 507
页数:12
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