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Epidermal Fatty Acid Binding Protein Mediates Depilatory-Induced Acute Skin Inflammation
Journal article   Open access   Peer reviewed

Epidermal Fatty Acid Binding Protein Mediates Depilatory-Induced Acute Skin Inflammation

Di Yin, Jiaqing Hao, Rong Jin, Yanmei Yi, Sobha R Bodduluri, Yuan Hua, Ajay Anand, Yibin Deng, Bodduluri Haribabu, Nejat K Egilmez, …
Journal of investigative dermatology, Vol.142(7), pp.1824-1834.E7
07/2022
DOI: 10.1016/j.jid.2021.11.040
PMCID: PMC9639752
PMID: 34942197
url
https://doi.org/10.1016/j.jid.2021.11.040View
Published (Version of record) Open Access

Abstract

Depilatory creams are widely used to remove unwanted body hair, but people with “sensitive skin” are subject to depilatory-induced skin burn/inflammation. It remains unknown what makes their skin more sensitive than others. Herein, we demonstrate that epidermal fatty acid binding protein (E-FABP) expressed in the skin plays a critical role in promoting depilatory-induced acute skin inflammation in mouse models. While Nair, a common depilatory cream, removed hair by breaking down keratin disulfide bonds, it activated cytosolic phospholipase A2 (cPLA2), leading to activation of the arachidonic acid (AA)/E-FABP/PPARβ signaling pathway in keratinocytes. Specifically, PPARβ activation induced downstream targets (e.g. COX2) and chemokine (e.g. CXCL1) production, which systemically mobilized neutrophils and recruited them to localize in the skin for acute inflammatory responses. Importantly, E-FABP deletion by CRISPR-Cas9 reduced cPLA2/PPARβ activation in keratinocytes, and genetic deletion of E-FABP protected mice from Nair-induced neutrophil recruitment and skin inflammation. Our findings suggest E-FABP as a molecular sensor for “sensitive skin” by triggering depilatory-induced, lipid-mediated skin inflammatory responses.

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