The mystery behind what makes us itch may finally have been solved. American researchers discovered that the presence of a common skin bacterium – Staphylococcus aureus – can make us itch by acting directly on our nerve cells.
The findings may help to explain why skin conditions such as eczema are often accompanied by a persistent and insatiable itch. In experiments on mice, scientists discovered the bacterium S. aureus made them develop an intensifying itch.
They identified the bacterial enzyme responsible for the itch by activating a protein involved in blood clotting, and when they gave the mice an existing anticlotting drug, it stopped their itch.
Additional tests on human cells have led researchers from the Harvard Medical School (HMS) in Boston, Massachusetts, to the belief that the anticlogging drug could become the basis for anti-itch creams.
The study, published in the journal Cell could therefore bring an end to the head-scratching mystery of the itch. Until now, the itch that frequently accompanies skin conditions such as eczema was believed to derive from the accompanying inflammation of the skin.
But these new findings suggest that S. aureus single-handedly causes the itch by instigating a molecular chain reaction that culminates in the urge to scratch.
When suffering from these skin conditions, the researchers say the equilibrium of microorganisms that keep our skin healthy is often thrown off balance, which allows the bacterium S. aureus to flourish.
“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,” said Dr. Isaac Chiu a senior author and an associate professor of immunology in the Blavatnik Institute at HMS.
“We show that itch can be caused by the microbe itself.” Itch can be quite debilitating in patients who suffer from chronic skin conditions.” added Dr. Liwen Deng study.
“Many of these patients carry on their skin the very microbe we’ve now shown for the first time can induce itch,” said Dr. Chiu’s Lab postdoctoral research.
Dr. Chiu’s team’s experiments showed that S. aureus releases a chemical that activates a protein on the nerve fibres that transmit signals from the skin to the brain.
Treating mice with an existing anti-clotting medicine successfully blocked the activation of the protein to interrupt this key step in the itch-scratch cycle – thus nullifying the urge to itch.
When researchers exposed the skin of mice to S. aureus, they developed an intensifying itch over the next several days, and the scratching that resulted from the itch caused worsening skin damage that spread beyond the original site of exposure.
The mice also became hypersensitive to innocuous stimuli that would normally not cause an itch. This hyperactive response, called ‘alloknesis’, is common in patients with chronic skin conditions accompanied by a persistent itch.
However, the response can also happen in people without any underlying conditions – as anyone who has experienced the scratchy feeling from wearing a wool sweater will attest to.
The researchers tested how the bacterium triggered an itch and found the bacterial enzyme protease V8 to be responsible.
Their continued analysis found that V8 triggers itch by activating the protein PAR1, which is found on skin neurons that originate in the spinal cord and carry various signals including touch, heat, pain, and itch from the skin to the brain.
PAR1 usually lies dormant, but when contacted with certain enzymes – including V8 – it becomes activated. Experiments in mice showed that once activated, PAR1 initiates a signal that the brain eventually perceives as an itch.
When researchers repeated the experiments with human neurons, they also responded to V8. “When we started the study, it was unclear whether the itch was a result of inflammation or not,” said Dr. Deng.
“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,” he added.
Because PAR1, the protein activated by S. aureus, is involved in blood clotting, the researchers tested whether an already approved anticlotting drug that blocks it would stop the itch – which it did.
The mice whose skin was exposed to S. aureus experienced rapid improvement following treatment with the drug, and their desire to scratch subsided dramatically.
As this PAR-blocking medication is already available and in use by humans, the researchers suggested its active ingredient could be repurposed as the basis for an anti-itch cream.
An immediate question that still begs an answer is whether other microbes can trigger an itch, which the researchers plan to answer in future work.
“We know that many microbes, including fungi, viruses, and bacteria, are accompanied by itch but how they cause itch is not clear,” said Dr. Chiu.
Beyond that, the HMS team will also strive for answers as to why a microbe would cause an itch, and whether there is some kind of evolutionary benefit for it.
One possibility is that pathogens may hijack itch and other neural reflexes to their advantage, similar to how previous research has shown that the TB bacterium directly activates neurons to cause cough, which might enable it to spread more easily from one host to another.
“It’s 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,” said Dr. Deng.
Why do we itch and scratch? Does it help us, or does it help the microbe? That’s something that we could follow up on in the future.
Produced in association with SWNS Talker
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