The Origins of Eczema May Start in the Uterus

During pregnancy, stress can elevate certain immune cells in the fetal skin and cause them to react excessively, typically around 6 to 8 months, potentially leading to eczema.

Skin mast cells, a type of immune cell, release histamines and other chemicals that result in redness, swelling, and itching during allergic responses. Though eczema is not classified as an allergy, these chemicals can instigate inflammatory flare-ups triggered by irritating substances like soaps, detergents, and diapers.

A series of studies on mice have demonstrated that mast cells become hypersensitized when exposed to stress hormones from the mother.

“What our findings indicate is that the emotional experiences of pregnant women can significantly impact their children’s health,” stated Nicolas Gaudenzio from the Toulouse Institute for Infectious and Inflammatory Diseases in France. “The sense of guilt for mothers is not the focus of this study; it may serve as a message for female partners and their support networks.”

Previous research has indicated a connection between maternal stress and eczema development in newborns. To investigate this further, Gaudenzio and his team conducted experiments with several pregnant mice.

Some mice underwent stress by being placed in a narrow tube exposed to bright light for 30 minutes over a span of 5 days. Researchers specifically targeted late third trimester periods, crucial for immune and nervous system development. They found heightened levels of stress hormones in the mice’s blood and amniotic fluid during this time.

After the mice gave birth, researchers simulated diaper-wearing by attaching saline-soaked pads to the backs of the hind knees and elbows to mimic common eczema-prone areas.

Offspring from stressed mothers predominantly displayed red, itchy, or scaly rashes in the targeted areas. In contrast, pups from control mothers, allowed to roam freely during pregnancy, exhibited only mild reactions without severe lesions.

Analysis of RNA sequences from sensory neurons connecting the skin to the spinal cord revealed nearly 300 differently expressed genes in the offspring of stressed mice. The puppies born to stressed mothers responded more aggressively to light touch, including being brushed with fine nylon fibers.

When immune cells from the skin of these puppies were sequenced, 500 genes showed differential expression in mast cells. Microscopically, these cells appeared primed to release histamine. “They were already in an active state in a neutral environment, indicating that the skin is predisposed to inflammation,” noted Gaudenzio.

Researchers repeated their experiments with pregnant mice treated to inhibit the production of corticosterone, a hormone integral to the stress response in rodents. They also administered additional corticosterone to unstressed pregnant mice, which resulted in their offspring developing eczema.

Moreover, genetically modified pups completely lacking certain immune responses did not develop eczema, even when their mothers were stressed.

This study represents a thorough and fascinating investigation,” commented Thomas Plum, a specialist in cell immunology at the German Cancer Research Center in Heidelberg. “It underscores the significance of interactions among immune cells, structural cells, and the nervous system at the tissue level.”

However, it’s essential to consider that these experiments were conducted in mice. “It’s an intriguing finding, but just the beginning,” Plum remarked.