Your skin forms memories. A bout of inflammation can train your skin to heal faster
Stem cells, which replenish the skin’s outer layer, take their cue from inflammation. Hence, a bout of inflammation sensitises cells and the next time around, it responds more rapidly.health Updated: Oct 19, 2017 15:12 IST
In a recent research, scientists have found that stem cells help skin close recurring wounds faster. The discovery could advance research and treatment of psoriasis and other inflammatory diseases. Inflammatory skin diseases are considered to be the most common problem in dermatology. These diseases come in many forms, from occasional rashes to chronic conditions such as dermatitis.
The researchers found that these stem cells, which replenish the skin’s outer layer, take their cue from inflammation, the body’s own response to injury or infection. The first bout of inflammation sensitises these cells: the next time they sense it coming on, they respond more rapidly. The scientists provide the first evidence that the skin can form memories of an inflammatory response.
“By enhancing responsiveness to inflammation, these memories help the skin maintain its integrity, a feature that is beneficial in healing wounds after an injury. This memory may also have detrimental effects, however, such as contributing to the relapse of certain inflammatory disorders such as psoriasis,” said Elaine Fuchs, the Rebecca C Lancefield Professor.
Whether burned by the sun, attacked by microbes, nicked by a paper cut or worse, the skin quickly becomes inflamed as the body seeks to halt the damage and initiate repair. It has long been known that the immune system maintains a memory of inflammation to mount faster responses to recurrent infections. But scientists in the Fuchs’ lab suspected that other types of long-lived cells might similarly remember inflammation.
In experiments with mice, Shruti Naik, a postdoc, and Samantha B. Larsen, a graduate student, showed that wounds closed more than twice as fast in skin that had already experienced inflammation than in skin that had never been damaged, even if that initial inflammatory experience had occurred as long as six months earlier, the equivalent of about 15 years for a human.
Inflammation can sometimes run amok, as happens in autoimmune diseases like psoriasis, a disorder marked by scaly, red patches that often flare up repeatedly in the same spot. Larsen said, “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.”
While taking about the study, Naik concluded, “A better understanding of how inflammation affects stem cells and other components of tissue will revolutionise our understanding of many diseases, including cancer, and likely lead to novel therapies.” The story was published in journal Nature.
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