IL-1 may be key in gut-skin inflammation link


Erythema nodosum, a condition often associated with colitis. Photo by:James Heilman, MD via Wikimedia Commons

Researchers say they have identified how inflammation in the gut can cause the immune system in the skin to lose tolerance for healthy bacteria, leading to inflammatory skin conditions.


The findings were published in Cell Reports.


In a press release from the University of California, San Francisco (UCSF), the study’s senior author dermatologist Dr. Tiffany Scharschmidt said: “What we learned is that factors involved with gut inflammation are actually causing the skin to react differently to the microbes it’s already become accustomed to.”


Dr. Scharschmidt is an Associate Professor of Dermatology in UCSF’s School of Medicine.


“The composition of bacteria on the skin didn’t change. Instead, what changed was the skin’s immune response to them,” she said.


Dr. Scharschmidt said that she believes this discovery may help explain skin disorders associated with colitis.


In the release, the authors note that typically the immune system tolerates commensal bacteria. However, in many forms of inflammatory bowel disease (IBD)—including colitis—a disruption in the immune-microbiome environment in the gut can disrupt this tolerance in the skin.


To understand this connection Dr. Scharschmidt and her colleagues induced colitis in a mouse model and observed how the immune system and microbiomes in the gut and skin changed in response.


The team found that inducing colitis in this way resulted in neutrophils infiltrating the skin of the mice. They write that this type of neutrophil infiltration of the skin has also been seen in humans with IBD-associated skin disorders. In the mouse model, activation of interleukin (IL)-1 was necessary for this infiltration to occur.


Colitis also seemed to unbalance the ratio of T-regulator (T-reg) to T-effector immune cells that respond to the common skin bacterium Staphylococcus epidermidis. With fewer T-reg cells, tolerance to the commensal bacterium was reduced and the T-effector cells increased immune response in the skin of the mouse models. However, this did not occur in model mice unresponsive to IL-1.


The study authors conclude these results show the importance IL-1 plays in driving immune intolerance to commensal bacteria and that therapies that could maintain the T-reg/T-effector balance could be worth investigating further.


“Understanding what’s going on in the skin is a first step towards thinking about new avenues to attack the problem,” said Dr. Scharschmidt.

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