Particulate matter 2.5 regulates lipid synthesis and inflammatory cytokine production in human SZ95 sebocytes

Abstract

A large body of evidence indicates that particulate matter (PM)2.5 is associated with various negative effects on human health. However, the impact and molecular mechanism of PM2.5 on the skin have not been elucidated. Therefore, the present study aimed to investigate the effects of two types of PM2.5 [water-soluble extracts (W-PM2.5) and non-water-soluble extracts (NW-PM2.5)] on cell proliferation, cell cycle progression, lipid synthesis, and inflammatory cytokine production of human SZ95 sebocytes. The results demonstrated that NW-PM2.5 and W-PM2.5 exposure dose-dependently inhibited SZ95 sebocyte proliferation by inducing G1 cell arrest. Furthermore, NW-PM2.5 and W-PM2.5 significantly reduced sebaceous lipid synthesis and markedly promoted the production of inflammatory cytokines, including interleukin-1α (IL-1α), IL-6 and IL-8 in SZ95 sebocytes. Additionally, the expression of aryl hydrocarbon (Ah) receptor (AhR), AhR nuclear translocator protein (ARNT), as well as cytochrome P450 1A1 were significantly increased following PM2.5 exposure. Thus, these findings indicate that PM2.5 exerts inhibitory effects on cell proliferation and lipid synthesis, and stimulatory effects on inflammatory cytokine production and AhR signaling activation in human SZ95 sebocytes.

The impact of airborne pollution on skin

“…In normal human epidermal keratinocytes (NHEKs) exposed to O 3 , activation of the aryl hydrocarbon receptor (AHR) induced the expression of several cytochrome P450 genes, including CYP1A1 . AHR activation and increased CYP1A1 expression have also been reported after exposure to B[a]P, PM 2.5 and water‐soluble tobacco smoke extracts …”

Negative Cellular Effects of Urban Particulate Matter on Human Keratinocytes Are Mediated by P38 MAPK and NF-κB-dependent Expression of TRPV 1

“…Ca 2+ influx and the expression of pro-inflammatory cytokines are important downstream events that are regulated by TRPV 1 [ 9 , 27 ], the expression of which is in turn upregulated by UPM treatment. In this study, the level of Ca 2+ influx and the expression levels of IL-8, TNF-α, and IL-1β were increased by UPM treatment.…”

“…A number of studies have shown that UPM affects several organs; including the cardiovascular and pulmonary systems [ 1 , 2 , 3 , 4 ], as well as several cell types including lung cells; macrophages; and epithelial cells [ 5 , 6 , 7 ]. In addition; epidemiological studies have shown that UPM exposure is correlated with several human diseases including bronchial asthma, chronic obstructive pulmonary disease, lung cancer, atherosclerosis, ischemic stroke, congestive heart failure, myocardial ischemia, and birth defects [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ].…”

Potential Role of NRF2 Agonist in Managing AHR-Mediated Chloracne by Dioxin

“…In accordance with the histopathology of chloracne, agonistic ligation of AHR accelerates epidermal terminal differentiation and keratinization [26][27][28]. Upon AHR stimulation, the proliferation and lipid synthesis of sebocytes are impaired, probably by the switching of sebocytes toward keratinocyte-like differentiation [21,29,30]. In this review, we focus on the AHR signaling related to chloracne and highlight its potential treatment using NRF2 agonist.…”