New research has found that stem cells residing in the skin can learn from earlier inflammatory episodes and heal faster when subsequently injured. This insight suggests a newly discovered relationship between inflammation and stem cells, and could have significant implications into how we understand not only skin conditions such as psoriasis, but a range of inflammatory disorders.

We have long known that our immune system harbors a strong memory of prior inflammatory events. This, of course, helps the body promptly respond to recurring infections. A team at The Rockefeller University set out to investigate whether other types of cells could foster this kind of inflammatory memory.

Skin was the team's first port of call but the scientists needed to focus on the deeper long-lived stem cells within the epithelium as most of our superficial skin cells don't last long enough to harbor a relevant memory.

The team showed that wounds in mice studies would heal up more than twice as fast in skin that had already suffered an earlier inflammatory episode. The rapid healing effect was seen in mice that had an initial inflammatory experience up to six months earlier, described as equivalent to about 15 years time in a human.

Uncovering the mechanism behind this skin cell memory the researchers revealed that an initial bout of inflammation prompted an increase in the expression of a gene called Aim2. This gene activates a protein that boosts the ability of skin stem cells to move into, and heal, a wound.

The research shows that a bout of inflammation physically opens up distinct sites that can activate the expression of this gene and these sites remain open after the skin has initially recovered. So when a second turn of inflammation strikes these genes are activated much faster leading to a wound healing faster.

As well as offering a novel insight into how our skin "remembers", this research suggests that recurrent inflammatory responses that affect other parts of the body could be propagated by more than just the immune system. Inflammatory disorders originating in the gut and bowel could be affected by this process as the linings of these areas are replenished by the same epithelial stem cells as found in our skin.

"Inflammatory diseases have long been blamed on immune cells that turn against the body. However, that is clearly not the only cause: Stem cells may also be important contributors," says Samantha B. Larsen, a graduate student working on the new study.

This understanding into the relationship between stem cells and inflammation will allow scientists entirely new ways to approach therapies for a variety of diseases, from superficial conditions such as psoriasis to more complex conditions including cancer.

The new research was published in the journal Nature.