What causes skin to itch? New research points a previously unknown factor

Surprisingly, even in situations with minimal inflammation, the mice still exhibited scratching behavior, indicating that the bacteria were directly affecting itch-producing nerve fibers. 

Scientists had prior knowledge of the association between S. aureus and eczema, but the specific connection was not clear. However, recent research has discovered that when S. aureus enters a mouse's skin, it releases an enzyme called V8. This enzyme activates a protein called PAR1, which is found on nerve cells in the skin. The activated protein then sends a signal to the brain, causing the mouse to feel itchy and prompting it to scratch.

Experiments involving in the laboratory using human nerve cells illustrated that the same mechanism could occur in humans, although it is not yet certain if these findings directly apply to people.

Nevertheless, this research could lead scientists in a new direction for developing treatments for eczema. Eczema affects approximately 10% of individuals in the United States, with the most common form being atopic dermatitis. This condition causes ongoing itchiness, dry and cracked skin, and is strongly linked to allergies like asthma or hay fever. 

According to Liwen Deng, a postdoctoral researcher in Chiu's lab and co-author of the study, it was found that nearly all of the lesions in patients with atopic dermatitis contain Staph aureus.

In the study, mice were directly exposed to S. aureus bacteria on their skin for several days. The researchers observed that by the third day, the mice developed skin irritation and by the fifth day, they scratched significantly more compared to mice who were not exposed to the bacteria. The affected mice also showed a higher likelihood of developing alloknesis, which is a condition where individuals experience itching from triggers that usually do not cause itching, such as gentle touch. To eliminate the possibility that inflammation was still responsible for the itch response, the research included mice with lower levels of immune cells or inflammatory chemicals associated with skin allergies. 

However, the results still indicated that the bacterium was the cause of the itchiness. 

According to Nathan Archer, an assistant professor of dermatology at Johns Hopkins University School of Medicine who was not involved in the research, the study successfully distinguished between the inflammatory response and the itch response. Dr. Peter Lio, the founding director of the Chicago Integrative Eczema Center, expressed in an email that the Harvard study strengthens the understanding of the role Staph bacteria play in causing itching sensations.

Lio further explained that the study revealed various toxins released by Staph, some causing inflammation, some damaging the skin barrier, and some directly leading to itchiness. Lio also was not involved in the research.

Archer commented that this study could provide important insights into the treatment of eczema patients who do not respond to current available treatments. Typically, doctors prescribe topical steroids or an injection for adults with moderate or severe eczema, which was approved in 2017.

Deng said that currently, there are no targeted treatments specifically addressing bacteria. 

She added that, in the future, scientists might develop a topical treatment that can prevent itchiness by blocking the S. aureus pathway. Another potential option would be to use Vorapaxar, an anti-clotting medication, to treat eczema as it is the only FDA-approved drug that can block the PAR1 protein.

The recent study showed that Vorapaxar appeared to decrease the urge to scratch in mice that received it.

Chiu suggested that this research could have implications for treating other skin conditions like impetigo, which causes red facial sores in infants and children, as long as Staph aureus is present on the skin. 

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