0
0
Scientists have made a groundbreaking discovery by pinpointing a common skin bacterium, Staphylococcus aureus, that triggers nerve cells in the skin. This activation prompts persistent scratching in individuals with skin conditions like eczema and atopic dermatitis.
These conditions often disrupt the natural balance of microorganisms essential for skin health, allowing S. aureus to thrive, as indicated by researchers from Harvard Medical School.
Until now, the itching associated with eczema and atopic dermatitis was thought to stem from skin inflammation. However, recent findings, derived from both mouse and human cell research and published in the journal Cell, reveal that S. aureus independently induces itch by setting off a molecular chain reaction that culminates in the urge to scratch.
Isaac Chiu, Associate Professor of immunology at HMS, remarked, “We’ve discovered a completely new mechanism behind itch—the bacterium Staph aureus, present in almost every patient with the chronic condition atopic dermatitis. We demonstrate that itch can be directly caused by the microbe itself.”
In experiments, mice exposed to S. aureus experienced escalating itchiness over several days, with repeated scratching leading to worsening skin damage extending beyond the original exposure site.
To understand how the bacterium triggers itch, researchers tested various modified versions of S. aureus lacking specific components of the bug’s molecular structure. They singled out a bacterial enzyme, protease V8, as the sole instigator of itch in mice.
Skin samples from atopic dermatitis patients exhibited higher levels of both S. aureus and V8 compared to healthy skin samples.
Their analysis revealed that V8 induces itch by activating a protein called PAR1 found on skin neurons originating in the spinal cord. These neurons transmit various skin signals—touch, heat, pain, and itch—to the brain. Normally dormant, PAR1 becomes activated upon contact with specific enzymes like V8.
The research demonstrated that V8 triggers PAR1 by altering one end of the protein, prompting a signal perceived by the brain as itch. Experiments in mice and human neuron-containing lab dishes verified this response to V8.
Administering an FDA-approved anti-clotting medication to animals successfully halted protein activation, interrupting this critical step in the itch-scratch cycle. This treatment alleviated symptoms and reduced skin damage.
These findings hold promise for the development of oral medications and topical creams targeting persistent itch linked to skin microbiome imbalances seen in conditions like atopic dermatitis, prurigo nodularis, and psoriasis.
