Researchers from Harvard Medical School have delved into the enigma of skin itching, specifically in conditions like eczema, and identified a potential culprit: Staphylococcus aureus (Source: NBC News).
Although inflammation is a known trigger for itchiness, a new study published in the journal Cell reveals that this bacterium can directly activate nerve cells in mice, leading to scratching even in situations with minimal inflammation.
Co-author of the study, Isaac Chiu, an associate professor of immunology at Harvard Medical School, expressed surprise at the 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 bacteria was directly acting on nerve fibers that produce itch.”
Prior to this research, the association between S. aureus and eczema was acknowledged, but the exact link remained unclear. The study demonstrated that when S. aureus invades a mouse’s skin, it releases an enzyme called V8, which activates a protein called PAR1 located on nerve cells in the skin. This activated protein then signals the brain, inducing an itching sensation and prompting the mouse to scratch.
While lab experiments involving human nerve cells confirmed a similar mechanism, researchers caution that the direct translation of these findings to humans is not yet certain. Nevertheless, the study provides a potential avenue for eczema treatments, impacting approximately 10% of the U.S. population.
“For patients with atopic dermatitis, almost all of their lesions harbor Staph aureus,” noted Liwen Deng, a postdoctoral researcher in Chiu’s lab and another co-author of the study.
The study exposed mice to S. aureus directly on the skin, leading to skin irritation and increased scratching compared to mice not exposed to the bacteria. It also revealed that the bacterium was responsible for inducing allokinesis, a condition where individuals itch from triggers that typically don’t cause itching.
While current treatments often focus on inflammation and skin barrier damage, this research hints at the possibility of developing topical treatments to block the S. aureus pathway or repurposing existing medications like Vorapaxar to address eczema by inhibiting the PAR1 protein.
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