Overview

• Using a late-gestation stress paradigm, pregnant mice had corticosterone spikes in blood and amniotic fluid, and their offspring developed lesions after mild mechanical or wet friction.
• Fetal skin mast cells were already degranulated at embryonic day 18.5, and mast cell–deficient mouse models were largely protected from the eczema-like phenotype.
• Blocking maternal corticosterone surges with metyrapone prevented abnormal mast cell activation and shielded offspring from lesions without altering dam or litter weights.
• Sensory neurons in offspring exhibited transcriptomic and anatomical changes linked to heightened touch and itch sensitivity, and these neuronal alterations persisted even when inflammation was prevented.
• The authors report transient features that resolved by week 24 in mice and note that human relevance remains unproven despite similar receptor expression patterns and observed higher early-gestation cortisol in some atopic pregnancies.