Cracking the itch mystery: New insights unveiled

S. aureus and itch-induced skin damage: The V8 protease-PAR1 axis revealed.

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Harvard Medical School scientists discovered that the typical skin bacterium Staphylococcus aureus can directly cause itch by affecting nerve cells. This breakthrough, observed in mice and human cells, was reported on November 22nd.

The recent research sheds light on the mystery of itch, particularly in common skin conditions like eczema and atopic dermatitis. It reveals that the bacterium Staphylococcus aureus, commonly found in these conditions, directly triggers itch by initiating a molecular chain reaction. This discovery challenges the previous belief that itch was solely a result of skin inflammation

The imbalance of microorganisms on the skin, often seen in conditions like eczema, allows Staphylococcus aureus to thrive and cause persistent itching. The study, led by senior author Isaac Chiu from Harvard Medical School, introduces a novel understanding of the mechanism behind the itch.

The study found that Staphylococcus aureus (S. aureus) releases a chemical triggering a nerve protein responsible for transmitting signals from the skin to the brain. Treating animals with an FDA-approved anticlotting medicine interrupted this process, breaking the itch-scratch cycle and relieving symptoms while minimizing skin damage. 

These insights could guide the development of oral medicines and creams for persistent itch-in conditions like atopic dermatitis and psoriasis, where an unbalanced skin microbiome is a factor. Chronic scratching in these conditions can lead to skin damage and increased inflammation, making effective treatments crucial.

To break the cycle of itch and scratching, researchers tested an anticlotting drug that blocks PAR1, the protein activated by Staphylococcus aureus. The drug showed quick success in mice exposed to S. aureus, reducing their urge to scratch and minimizing skin damage. 

Additionally, once treated, the mice no longer experienced abnormal itching from harmless stimuli. The PAR1 blocker, already used to prevent human blood clots, holds promise as an anti-itch medication. Researchers suggest it could be repurposed for topical creams. Future studies will explore whether other microbes, such as fungi and viruses, can trigger itch.

The discovery prompts a broader question: Why would a microbe induce itch? The researchers propose that pathogens might exploit itch and other neural reflexes for their benefit. For instance, previous studies have revealed that the TB bacterium activates neurons to cause coughing, potentially aiding its transmission from one host to another.

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

Harvard Medical School’s research sheds light on the intricate mechanisms of itch. It opens avenues for potential treatments and medications targeting the underlying causes. The findings challenge traditional perspectives on itch, urging further exploration into the intricate interplay between microbes and sensory responses.

Journal reference:

  1. Liwen Deng, Flavia Costa et al., aureus drives itch and scratch-induced skin damage through a V8 protease-PAR1 axis. Cell. DOI: 10.1016/j.cell.2023.10.019.

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