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UK and Japanese scientists discover skin bacteria lipopeptides that inhibit IL-33, offering potential eczema treatment

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Friendly Skin Bacteria May Hold the Key to Preventing Eczema

A new study published in Nature Communications reveals that benign bacteria living on our skin naturally produce compounds that could stop eczema before it starts.

Friendly skin bacteria release lipopeptides which can prevent eczema development in mice by blocking Interleukin-33 (IL-33) release.

How It Works

As friendly staphylococcal species age and their nutrient supply runs low, they release small molecules called lipopeptides. These molecules act directly on skin cells (keratinocytes), preventing them from releasing a key driver of allergic inflammation known as Interleukin-33 (IL-33).

Key discoveries from the study:

  • Only specific lipopeptides work: Diacylated lipopeptides were effective at blocking IL-33, while monoacylated versions had no effect.
  • A molecular trap: The lipopeptides do not destroy IL-33. Instead, they block it from leaving the nucleus, effectively trapping it in the perinuclear space and preventing the inflammatory response.
  • The counterpoint: The same research team previously showed that a protein (Sbi) from the harmful Staphylococcus aureus bacteria triggers IL-33 release and eczema flare-ups.
What the Researchers Say

Dr. Peter Arkwright (University of Manchester):

"Lipopeptides are small, stable, non-infectious chemical structures with potential as topical treatment for eczema, and possibly other allergic diseases like hay fever."

Dr. Joanne Pennock (University of Manchester):

"The findings explain how exposure to diverse microbes early in life may reduce allergy risk."

Professor Akane Tanaka (Tokyo University of Agriculture and Technology):

"Blocking IL-33 with a biologic drug stops eczema in mice; now bacteria can do it themselves."

Professor Hiroshi Matsuda (Tokyo University of Agriculture and Technology):

"The findings overturn assumptions about bacterial molecules; next step is testing in humans."

Funding

The study was supported by the Leo Foundation and the Japan Society for the Promotion of Science.