Scientists have exposed the true culprit behind the itchy sensation that accompanies common skin conditions, in a discovery that might help break the itch-scratch cycle.
Common bacteria – Staphylococcus aureus – triggers a chemical chain reaction in nerve cells, driving the irritating sensation and urge to scratch, according to a study by Harvard Medical School researchers published in Cell.
The bacterium releases an enzyme called protease V8. This activates a protein on nerve fibres, sending a signal from the skin to the brain, culminating in an itchy feeling.
The study in mice and human cells helps explain the persistent itching associated with chronic skin conditions like eczema and atopic dermatitis, symptoms previously thought to be caused by inflammation.
“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. We show that itch can be caused by the microbe itself,” says Associate Professor of Immunology Isaac Chiu, an author of the paper.
Conditions like eczema, atopic dermatitis and psoriasis lead to an imbalance in the skin’s microorganisms allowing Staph aureus to flourish.
Skin samples from people with atopic dermatitis had higher levels of both the bacterium and the enzyme (protease V8) than those with healthy skin.
Once bacteria triggers an itch, it creates the desire to scratch, and that can lead to skin damage and inflammation.
The study finds treating mice with an anti-clotting medicine successfully blocked the activation of the protein (which is usually associated with clotting), relieving symptoms and minimising skin damage, and may inform the design of treatments in humans.
Further research is required to determine whether there are other bacteria, beyond Staph aureus, also capable of causing an itch.
Originally published by Cosmos as What causes an itch?
Petra Stock
Petra Stock is a journalist and engineer. She has previously worked in climate change, renewable energy, environmental planning and Aboriginal heritage policy.
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