Scientists Find an Unexpected Trigger of Eczema – And Clues on How to Stop It : ScienceAlert

The unbearable itch that accompanies the chronic inflammatory skin condition eczema has a new culprit.

Scientists have discovered that a familiar bacteria, Staphylococcus aureus, ignites persistent itches by directly triggering sensory neurons in the skin, a finding that could help researchers devise new treatments.

Eczema, which is also known as atopic dermatitis, is common in children and teenagers but also affects one in ten adults.

Up until now, immune cells and the inflammatory molecules they secrete were thought to be the main drivers of the insufferable itch that occurs with eczema. That itch so often drives a vicious urge to scratch which only damages the skin further, leaving it red, raw, swollen, and cracked.

Years ago, researchers figured out that people lacking a skin protein called filaggrin were more likely to develop eczema; but what specifically caused the itch that enflames eczema still bugged them.

Now, a team of mostly US researchers has shown in a series of animal experiments how S. aureus, a bacterium that infiltrates broken skin to cause infections, single-handedly causes itching by setting off sensory nerve cells in the skin surface.

“We’ve identified an entirely novel mechanism behind itch – the bacterium Staph aureus, which is found on almost every patient with the chronic condition atopic dermatitis,” says Isaac Chiu, an immunologist at Harvard Medical School. “We show that itch can be caused by the microbe itself.”

Mice were wrapped in gauze loaded with S. aureus to model eczema in humans. The animals exposed to S. aureus scratched their sores, and the researchers found the bacteria congregated close to sensory nerve endings in the now-inflamed outer skin, the epidermis.

To figure out how the bacteria might be acting on those nerves, the researchers systematically tested different strains of S. aureus engineered to lack specific components of the microbe’s molecular arsenal.

After ruling out nine others, Chiu and colleagues found one enzyme that S. aureus releases on contact with skin, protease V8, triggered itching behaviors in the mice by activating another protein, PAR1, which set off the sensory neurons.

When exposed to S. aureus devoid of V8, the mice didn’t scratch nearly as much, and their skin was less flaky and irritated. And when animals were treated with a drug that blocks PAR1, their symptoms also eased.

Further experiments ruled out immune cells as the instigators of the animals’ itch. Mice depleted of mast cells and basophils, two types of immune cells implicated in itches and allergies, kept on scratching after exposure to S. aureus.

“You don’t necessarily have to have inflammation for the microbe to cause itch, but that itch exacerbates inflammation on the skin,” explains Liwen Deng, lead author and microbiologist at Harvard Medical School.

If validated in human studies, the findings could present a clear target for alleviating eczema’s endless itch that can deprive some patients of sleep.

Most current eczema treatments try to soothe the skin, calm the immune system, and restore the skin barrier without clearing up the condition entirely – though researchers have clued on to the idea that targeting skin bacteria might provide lasting relief.

The PAR1 blocker tested in this study is already used to prevent blood clots in humans so it could be repurposed. Like the mice, skin samples from patients with atopic dermatitis had higher V8 levels and more S. aureus than healthy skin, but further testing is required.

Future studies could also investigate if pathogens like S. aureus hijack itchy sensations to facilitate their spread.

“It’s a speculation at this point, but the itch-scratch cycle could benefit the microbes and enable their spread to distant body sites and to uninfected hosts,” Deng says.

The study has been published in Cell.