Ann Dermatol.
2020 Dec;32(6):496-507. 10.5021/ad.2020.32.6.496.
Effects of Particulate Matter in a Mouse Model of Oxazolone-Induced Atopic Dermatitis
- Affiliations
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- 1Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Korea
- 2Department of Dermatology, Nowon Eulji Medical Center, Eulji University, Seoul, Korea
- 3Department of Dermatology, Seoul National University Hospital, Seoul, Korea
- KMID: 2508673
- DOI: http://doi.org/10.5021/ad.2020.32.6.496
Abstract
- 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.
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