205 Topical application of Bisphenol A leads to atopic dermatitis-like features

In the past decades, incidence of atopic dermatits (AD) has been increasing in adult population, raising question potential environmental triggers. We hypothesized that pollution might be a contributing factor. Bisphenol A (BPA) is an endocrine disruptor with unkown pathophysiological consequences its repeated skin exposure. aimed to decipher effects topical application BPA onto human epidermal equivalents (HEEs) generated keratinocytes isolated from healthy biopsies. parallel, we HEEs made AD patients’ biopsies for comparison BPA-treated HEEs. Results showed increased mRNA level pro-inflammatory mediators including IL-1a, IL1b, IL-6, IL-8 and CCL17 both Furthermore, SOD2, SOD1 VDAC were increased, indicating cellular oxidative stress. Indeed, cytochrome P450 (CYP) activity produces ROS excessive amounts. line this, CYP1A1, CYP3A4, UGT1A1, PXR upregulated. Effects mediated via signaling because rifampicin-treated exhibit similar features than those treated BPA. Moreover, reduced corneodesmosin biotin-diffusion assay impaired tight junctions, suggesting abnormal barrier formation. To confirm these results vivo, mice topically show TEWL, impairment. ear thickness edema acanthosis. systemic Th2-dominant inflammation, dermal infiltration mast cells. conclusion, exposure provokes defect elicits inflammation resembling AD. This result activation xenobiotic metabolism, production