Abstract
The molecular mechanisms that underlie the detrimental effects of particulate matter (PM) on skin barrier function are poorly understood. In this study, the effects of PM2.5 on filaggrin (FLG) and skin barrier function were investigated in vitro and in vivo. The levels of FLG degradation products, including pyrrolidone carboxylic acid, urocanic acid (UCA), and cis/trans-UCA, were significantly decreased in skin tape stripping samples of study subjects when they moved from Denver, an area with low PM2.5, to Seoul, an area with high PM2.5 count. Experimentally, PM2.5 collected in Seoul inhibited FLG, loricrin, keratin-1, desmocollin-1, and corneodesmosin but did not modulate involucrin or claudin-1 in keratinocyte cultures. Moreover, FLG protein expression was inhibited in human skin equivalents and murine skin treated with PM2.5. We demonstrate that this process was mediated by PM2.5-induced TNF-α and was aryl hydrocarbon receptor dependent. PM2.5 exposure compromised skin barrier function, resulting in increased transepidermal water loss, and enhanced the penetration of FITC-dextran in organotypic and mouse skin. PM2.5-induced TNF-α caused FLG deficiency in the skin and subsequently induced skin barrier dysfunction. Compromised skin barrier due to PM2.5 exposure may contribute to the development and the exacerbation of allergic diseases such as atopic dermatitis.
Highlights
Particulate matter (PM) is one of the major air pollutants and a major health concern that continues to grow with industrialization and urbanization [1,2,3]
Skin FLG degradation products (FDPs) levels are decreased in subjects who live in a high-PM2.5 environment
The major components of polycyclic aromatic hydrocarbons (PAHs) in Seoul and Denver were similar, and the average levels of PAHs during the winter season, according to the published data, are 16.1 ± 10.1ng/m3 and 3.1 ± 0.4 ng/m3 in Seoul and Denver, respectively [30,31,32]. This shows that the levels of PM2.5 and PAHs were about 5 times higher in Seoul, Korea, as compared with Denver, Colorado, USA
Summary
Particulate matter (PM) is one of the major air pollutants and a major health concern that continues to grow with industrialization and urbanization [1,2,3]. The majority of the particle mass is in the fraction with less than 2.5 μm, and these particles can carry a large amount of absorbed pollutants, oxidants, and organic compounds [6]. Jin et al reported that PM penetrates the epidermis through hair follicles in normal, intact skin and causes cutaneous inflammation in a mouse model [7]. It has been reported that polycyclic aromatic hydrocarbons (PAHs), major components of PM2.5, penetrate the skin in animal models because of their lipophilic nature [1, 8,9,10]. PAHs have been shown to activate aryl hydrocarbon receptors (AHRs) while binding to the AHR in cytoplasm, induce translocation of AHR to the cell nuclei to regulate cellular gene expression [11, 12]
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