Researchers developed a potential way to disrupt chronic inflammation of multiple sclerosis in the lab of Alban Gaultier, of the University of Virginia School of Medicine’s Department of Neuroscience and its Center for Brain Immunology and Glia.
Feb. 15 (UPI) -- New research suggests it could be possible to disrupt the inflammation that causes multiple sclerosis by blocking a specific cell receptor, according to a study published Wednesday in the scientific journal PLOS Biology.
The study, performed in the lab of Alban Gaultier, an associate professor of neuroscience at the University of Virginia's School of Medicine's Department of Neuroscience's Center for Brain Immunology and Glia, gives insight into the link between an immune system regulator and MS.
"We are approaching the search for multiple sclerosis therapeutics from a new direction," said Andrea Merchak, a doctoral candidate in neuroscience, who performed the study with colleagues.
The disease is caused by the immune system attacking the myelin protective sheath that covers nerve cells. When myelin is damaged, it interferes with the ability for the brain to communicate with nerves in the body.
Scientists are unsure what exactly causes MS, but believe that the microbiome of the gut is related to the condition.
"UVA's new findings bolster that, determining that an immune system controller found in "barrier tissues" such as the intestine plays a vital role in the disease. This regulator can reprogram the gut microbiome to promote harmful, chronic inflammation, the researchers found," according to a university press release.
Nearly 1 million Americans suffer from MS, according to the National Multiple Sclerosis Society. While treatment options exist, and many MS patients can lead normal lives with treatment, the diseases can result in severe symptoms like loss of motor control and death.
Researchers believe the ability to block receptors within cells offers a path to new treatments.
"Gaultier and his collaborators blocked the activity of the regulator, called "aryl hydrocarbon receptor," in immune cells called T cells and found that doing so had a dramatic effect on the production of bile acids and other metabolites in the microbiomes of lab mice. With this receptor out of commission, inflammation decreased and the mice recovered," the release said.
"Due to the complexity of the gut flora, probiotics are difficult to use clinically. This receptor can easily be targeted with medications, so we may have found a more reliable route to promote a healthy gut microbiome," Merchak said.
"Ultimately, fine-tuning the immune response using the microbiome could save patients from dealing with the harsh side effects of immunosuppressant drugs," she said.
