Abstract
Peroxisome proliferator‐activated receptors (PPARs) are a family of nuclear hormone receptors. In skin, PPARs modulate inflammation, lipid synthesis, keratinocyte differentiation and proliferation and thus are important for skin barrier homeostasis. Accordingly, PPAR expression is altered in various skin conditions that entail epidermal barrier impairment, that is atopic dermatitis (AD) and psoriasis. Using human epidermal equivalents (HEEs), we established models of acute epidermal barrier impairment devoid of immune cells. We assessed PPAR and cytokine expression after barrier perturbation and examined effects of keratinocyte‐derived cytokines on PPAR expression. We show that acetone or SDS treatment causes graded impairment of epidermal barrier function. Furthermore, we demonstrate that besides IL‐1β and TNFα, IL‐33 and TSLP are highly relevant markers for acute epidermal barrier impairment. Both SDS‐ and acetone‐mediated epidermal barrier impairment reduce PPARG expression levels, whereas only SDS enhances PPARD expression. In line with findings in IL‐1β and TNFα‐treated HEEs, abrogation of IL‐1 signalling restores PPARG expression and limits the increase of PPARD expression in SDS‐induced epidermal barrier impairment. Thus, following epidermal barrier perturbation, keratinocyte‐derived IL‐1β and partly TNFα modulate PPARG and PPARD expression. These results emphasize a role for PPARγ and PPARβ/δ in acute epidermal barrier impairment with possible implications for diseases such as AD and psoriasis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.