TY - JOUR
T1 - Epidermal Fatty Acid‒Binding Protein Mediates Depilatory-Induced Acute Skin Inflammation
AU - Yin, Di
AU - Hao, Jiaqing
AU - Jin, Rong
AU - Yi, Yanmei
AU - Bodduluri, Sobha R.
AU - Hua, Yuan
AU - Anand, Ajay
AU - Deng, Yibin
AU - Haribabu, Bodduluri
AU - Egilmez, Nejat K.
AU - Sauter, Edward R.
AU - Li, Bing
N1 - Publisher Copyright:
© 2021 The Authors
PY - 2022/7
Y1 - 2022/7
N2 - 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. In this study, we show 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. Although a depilatory cream removed hair by breaking down keratin disulfide bonds, it activated cytosolic phospholipase A2, leading to activation of the arachidonic acid/E-FABP/peroxisome proliferator–activated receptor β signaling pathway in keratinocytes. Specifically, peroxisome proliferator–activated receptor β activation induced downstream targets (e.g., cyclooxygenase 2) 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 cytosolic phospholipase A2/peroxisome proliferator–activated receptor β activation in keratinocytes, and genetic deletion of E-FABP protected mice from depilatory cream-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.
AB - 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. In this study, we show 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. Although a depilatory cream removed hair by breaking down keratin disulfide bonds, it activated cytosolic phospholipase A2, leading to activation of the arachidonic acid/E-FABP/peroxisome proliferator–activated receptor β signaling pathway in keratinocytes. Specifically, peroxisome proliferator–activated receptor β activation induced downstream targets (e.g., cyclooxygenase 2) 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 cytosolic phospholipase A2/peroxisome proliferator–activated receptor β activation in keratinocytes, and genetic deletion of E-FABP protected mice from depilatory cream-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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U2 - 10.1016/j.jid.2021.11.040
DO - 10.1016/j.jid.2021.11.040
M3 - Article
C2 - 34942197
AN - SCOPUS:85124136883
SN - 0022-202X
VL - 142
SP - 1824-1834.e7
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 7
ER -