In a press release from Harvard Medical School, researchers detailed new research into the potential causes behind itch in patients with skin conditions. In a new study published by Deng et al in Cell, they analyzed the effects of Staphylococcus aureus bacteria—commonly found on the skin—in mouse models and human cells. The researchers noted that mice that were exposed to S aureus developed severe itch within several days, which was worsened by repeated scratching. Further, innocuous stimuli such as a light touch were more likely to trigger abnormal itch in the exposed mice. The observed hypersensitive response, known as alloknesis, is prevalent among patients with eczema and atopic dermatitis. To elucidate the link between the bacteria and itch, the researchers evaluated 10 enzymes released by the S aureus bacteria upon contact with the skin and established a correlation between the protease V8 enzyme and intensified itch in the mouse model. The researchers revealed that S aureus may activate the PAR1 protein present in skin neurons, which is responsible for transmitting touch, heat, pain, and itch signals from the skin to the brain. Human neuron samples exposed to the protease V8 enzyme were also activated. The researchers hypothesized that the unbalanced skin microbiome present in patients with eczema and atopic dermatitis may prompt S aureus bacteria to proliferate by increasing itch to help it spread to other areas of the skin. After treating the exposed mice with PAR1 blockers, a U.S. Food and Drug Administration (FDA)-approved anticlotting agent, the researchers demonstrated a reduction in the itch-scratch cycle and minimized skin damage. These new findings may illuminate factors contributing to persistent itch in patients with eczema and atopic dermatitis, and may lead to the development of novel targeted oral and topical treatments to help manage skin conditions characterized by itch.