cis-vaccenic-acid and Dermatitis

Mechanical damage on the skin not only affects barrier function but also induces various immune responses, which trigger or exacerbate skin inflammation. However, how mechanical damage-induced skin inflammation is regulated remains incompletely understood. Here, we show that keratinocytes express the long-chain fatty-acid elongase Elovl6. Mice deficient in Elovl6 showed higher levels of cis-vaccenic acid (CVA) in the epidermis and severe skin inflammation induced by mechanical damage due to tape stripping than did wild-type mice. CVA accelerated tape stripping-triggered keratinocyte death and release of danger-associated molecular patterns (DAMPs) such as high-mobility group box 1 protein (HMGB-1) and IL-1α, which induced production of proinflammatory cytokines and chemokines IL-1β and CXCL-1 by keratinocytes. Our results demonstrate that Elovl6 regulates mechanical damage-triggered keratinocyte death and the subsequent dermatitis.

Topics: Acetyltransferases; Animals; Biomechanical Phenomena; Cell Death; Chemokine CXCL1; Dermatitis; Epidermis; Fatty Acid Elongases; Gene Expression Regulation; HMGB1 Protein; Interleukin-1alpha; Interleukin-1beta; Keratinocytes; Mechanotransduction, Cellular; Mice; Mice, Inbred C57BL; Mice, Knockout; Oleic Acids