Friendly skin bacteria could hold the key to stopping eczema in its tracks according to a breakthrough by a team of UK and Japanese scientists.
Their new study reveals harmless microbes living on our skin release powerful molecules that can shut down the inflammatory chaos triggered by Staphylococcus aureus, the bug long known to wreak havoc in eczema.
Based at The University of Manchester and Tokyo University of Agriculture and Technology, they found that when nutrients run low, many friendly staphylococcal species release tiny lipopeptides as they age that calm the skin's immune response.
The lipopeptides stop keratinocytes - the skin's frontline cells - from pumping out Interleukin-33 (IL‑33), a major driver of allergic inflammation.
The discovery, they say, potentially open the door to a new class of safe, stable, non‑infectious treatments that could help millions living with skin and other allergic diseases.
The findings are the latest breakthrough by the team, after previously showing that a protein released by Staphylococcus aureus, known as Sbi, triggers IL-33 and sparks eczema flare‑ups. Applying the lipopeptides to the skin of mice prevented IL‑33 release and stopped eczema from developing.
Certain types of lipopeptides - diacylated were the most effective, while another type - monoacylated versions had no effect. The molecules blocked IL‑33 from leaving the nucleus, trapping it in the perinuclear space- the gap between the inner and outer membranes of the nucleus and preventing it from fuelling inflammation.
The new findings- published in the journal Nature Communications today - confirm their suspicion that good bacteria might naturally counteract this effect.
Study author Dr Peter Arkwright from The University of Manchester said: "We think this is a very exciting result as lipopeptides are small, stable, non-infectious chemical structures that have the potential to be used as a topical treatment for eczema. They might also be used in the future to treat other allergic diseases such as hay fever."
Study author Dr Joanne Pennock from The University of Manchester commented: "For years we've known that children raised around farm animals or exposed to diverse microbes early in life are less likely to develop allergies, but we haven't understood the precise mechanisms behind this protection.
Study author Professor Akane Tanaka from Tokyo University of Agriculture and Technology said: "We have previously already shown that blocking IL‑33 with a biologic drug stops eczema in the same mouse model. Now we've shown that bacteria can do it themselves- an exciting and potentially game-changing discovery."
Study author Professor Hiroshi Matsuda from Tokyo University of Agriculture and Technology said: "Our findings overturn long‑held assumptions about how bacterial molecules behave. Instead of triggering immune alarms through TLR pathways, these lipopeptides bypass them entirely. The next step is testing these lipopeptides in people with eczema to see if they can be turned into real‑world treatments."
The study was supported by the Leo Foundation and the Japan Society for the Promotion of Science
