The damage that intestinal inflammation can cause extends beyond the digestive system, even affecting the skin. This is the conclusion reached by researchers from the University of California, San Francisco, and the key to this reaction lies in the gut microbiome. It has already been shown that changes in the microbiome have been associated with an increased risk of various diseases, such as asthma, rheumatoid arthritis, and multiple sclerosis.
The study was published in Cell Reports and the research team looked at how ulcerative colitis, the chronic inflammation of the large intestine, can cause painful and persistent skin conditions that look like skin infections, but don’t actually contain skin pathogens.
What the study researchers found is that the factors associated with gut inflammation actually cause skin reactions to the microbes it is already used to. The composition of bacteria on the skin did not change. Instead, what changed was the skin’s immune response to them.
Immune system and gut microbiome are inextricably linked and the disturbance of the latter can also lead to skin changes. This phenomenon occurs in a number of conditions, including ulcerative colitis, which fall under the umbrella of inflammatory bowel disease (IBD).
Mice and their reactions
The researchers performed some experiments on mice and focused on the ulcerative colitis phenomenon, observing how the immune system and the microbiome in the gut and skin responded.
It was found that neutrophils, a type of inflammatory immune cell, infiltrated the skin. This invasion, which has also been seen in people with IBD-related skin conditions, required the activity of interleukin 1 (IL-1), a protein that plays a role in regulating the immune response.
The researchers’ second striking discovery involved the ability of ulcerative colitis to reverse tolerance to specific skin bacteria, triggering inflammatory responses of the immune system against the good bacteria.
The body’s tolerance to bacteria is maintained by balancing two types of immune cells that have opposing functions. T-regulatory cells promote tolerance, while T-effector cells defend against microbes that do not belong in the body. Tolerance occurs when T-regulatory cells control effectors.
By looking at how T-cells target the harmless skin bacterium Staphylococcus epidermidis, the researchers concluded that ulcerative colitis led to a lower ratio of regulatory cells to their effector counterparts. As a result, this deficiency led to skin inflammation.
The researchers then performed one more experiment in mice, inducing ulcerative colitis in a group of mice whose T-cells did not respond to IL-1. In contrast to the reaction of normal mice, the second group of mice showed no accumulation of neutrophils in the skin. Therefore, the ratio of the two types of T-cells was not affected and no inflammation occurred.
Finally, treatments that could balance the T-cell response are quite promising and may open new avenues in the treatment of skin diseases, according to the researchers.
