Palmitic acid aggravates atopic dermatitis by regulating SGK1/NEDD4L-involved cutaneous neuroimmune inflammation through driving TRPV1 and MRGPRB2 S-palmitoylation.

ABSTRACT:

Objective

To determine how cutaneous palmitic acid (PA) modulates transient receptor potential vanilloid-1(TRPV1) in nociceptor and dorsal-root-ganglions (DRGs), and Mas-related G protein-coupled receptor B2 (MRGPRB2) in mast cells (MCs), and to investigate their associations with serum- and glucocorticoid-regulated kinase-1 (SGK1)/neural precursor cell expressed developmentally down regulated 4-like (NEDD4L) in atopic dermatitis (AD).

Methods

AD was induced in mice with nedd4l or sgk1 conditional knock-out(cKO) in nociceptor, mrgprb2, nedd4l, or sgk1 cKO in MCs. Intradermal PA, substance P(SP), or pan-palmitoylation inhibitor 2BP was administered. Isolated DRGs and mouse bone-marrow-derived-MCs (mBMMCs) were used.

Results

Cutaneous PA levels were increased in AD mice

SUBMITTER: Chen B 

PROVIDER: S-EPMC12862028 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature