November 23, 2023
The mystery of why skin conditions, particularly eczema, lead to persistent itching has long perplexed scientists. While inflammation has been a known contributor, a groundbreaking study published on Wednesday in the journal Cell has unveiled a previously unknown trigger for itchiness: a bacterium named Staphylococcus aureus.
Conducted by researchers from Harvard Medical School, the study demonstrated that this bacterium could directly activate nerve cells in mice, shedding light on a novel mechanism for itch induction. Isaac Chiu, an associate professor of immunology at Harvard Medical School and co-author of the study, expressed surprise at their findings, stating, “What was surprising is that in some situations where there was very little inflammation, we could still see the mice scratching. It turns out, the reason is that the bacteria was directly acting on nerve fibers that produce itch.”
The study focused on the association between S. aureus and eczema, a connection acknowledged in the scientific community but not thoroughly understood until now. The researchers discovered that once S. aureus invades a mouse’s skin, it releases an enzyme called V8. This enzyme activates a protein called PAR1 located on nerve cells in the skin, sending a signal to the brain that triggers itching and prompts the mouse to scratch.
While lab experiments involving human nerve cells supported the possibility of a similar mechanism in people, the direct translation of these findings to humans is yet to be confirmed.
The implications of this research extend to potential advancements in eczema treatments, offering a new avenue for exploration. Eczema affects approximately 10% of the U.S. population, with the most common type, atopic dermatitis, causing chronic itching, dryness, and cracked skin, often associated with allergies like asthma or hay fever.
Liwen Deng, a postdoctoral researcher in Chiu’s lab and co-author of the study, emphasized the prevalence of Staph aureus in patients with atopic dermatitis, stating, “For patients with atopic dermatitis, almost all of their lesions harbor Staph aureus.”
In the study, mice exposed to S. aureus on their skin developed skin irritation by the third day, with a significant increase in scratching observed by the fifth day compared to a control group.
The research also explored the possibility that inflammation might be driving the itch response, but results involving mice with lower levels of immune cells or inflammatory chemicals suggested that the bacterium was the primary cause of itchiness.
Nathan Archer, an “assistant professor of dermatology at Johns Hopkins University School of Medicine,” who was not involved in the study, commended the research for dissecting the inflammatory and itch responses, providing important clues for treating eczema patients resistant to current treatments.
The study proposes potential treatment avenues, including the development of a topical treatment blocking the S. aureus pathway or repurposing Vorapaxar, an anti-clotting medication, to target the PAR1 protein. In the study, Vorapaxar showed promise in reducing the desire to scratch in mice.
Isaac Chiu suggested broader applications for the research, indicating relevance to skin conditions beyond eczema, such as impetigo, an infection causing red facial sores in infants and children, wherever Staph aureus may be present on the skin.