Researchers have identified a potential cause of chronic itching in patients with conditions like eczema, linking it to a common bacterium carried by one in three Americans.
Previously, scientists attributed persistent itching in individuals with skin conditions to inflammation.
However, a groundbreaking study conducted at Harvard University reveals that itching associated with eczema may result from a different mechanism altogether.
In pioneering research involving mice and human cells, Harvard University scientists found that a typically benign strain of bacteria residing in the nose and skin, Staphylococcus aureus, can infiltrate skin cells and induce an uncontrollable urge to scratch.
Dr. Isaac Chiu, immunology professor at Harvard Medical School and study author, explained, “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.”
These findings hold promise for the development of new topical treatments aimed at alleviating chronic itching in patients with eczema and similar conditions.
In individuals with eczema, disturbances in the skin’s microbiome — the healthy bacteria and oils that protect it — disrupt the balance, allowing harmful bacteria like Staphylococcus aureus to thrive.
Although typically harmless, this bacterium is known to cause staph infections, which can lead to skin infections, food poisoning, and potentially life-threatening bloodstream infections if they enter the bloodstream.
The study involved swabbing the skin on both arms of 14 healthy participants and 13 eczema patients aged 18 to 58 years. Mice exposed to Staphylococcus aureus developed intense itching that worsened over several days, resulting in skin damage.
Researchers modified different strains of Staphylococcus aureus to pinpoint which enzymes triggered the itch.
They discovered that an enzyme called V8 acts like molecular scissors, cleaving part of the PAR1 protein that lines skin neurons.
This action prompts PAR1 to transmit signals through the neurons to the brain, triggering the urge to scratch.
Dr. Liwen Deng, lead study author and postdoctoral researcher in Dr. Chiu’s lab, highlighted, “When we started the study, it was unclear whether the itch was a result of inflammation or not.
We show that these things can be decoupled, that you don’t necessarily have to have inflammation for the microbe to cause itch, but that the itch exacerbates inflammation on the skin.”
To test their findings further, researchers administered an FDA-approved anti-clotting medication to mice with itch symptoms, blocking PAR1’s activation. This significantly reduced the urge to scratch and minimized skin damage caused by itching.
The study’s implications could lead to the development of topical creams to mitigate itching and prevent long-term skin damage in the 10% of Americans affected by eczema.
Looking ahead, researchers plan to investigate if other bacteria play a role in causing itching in patients with skin conditions.
Dr. Chiu emphasized, “We know that many microbes, including fungi, viruses, and bacteria, are accompanied by itch, but how they cause itch is not clear.”
Dr. Deng added, “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.”
Understanding the mechanisms behind itching could open doors to innovative treatments and a deeper comprehension of how microbial interactions affect human health.
