Neuroscientists at the University of Virginia Health System (UVA) in the US have discovered a potential way to interrupt the chronic inflammation responsible for multiple sclerosis (MS).
The new UVA study identifies an essential factor in the hyperactive autoimmune response and the neuroinflammation which are the hallmarks of MS. Blocking this axis in a research model of MS alleviated harmful inflammation, providing researchers with a prime target in their efforts to develop new treatments for multiple sclerosis and other autoimmune diseases.
The investigation was carried out by Andrea Merchaka doctoral candidate in neuroscience, and colleagues in the laboratory of Dr. Alban Gaultier, Department of Neuroscience at the University of Virginia School of Medicine and its Center for Brain Immunology and Glia (BIG).
“We are approaching the search for multiple sclerosis therapies from a new direction,” says Merchak. The researcher also explains that, by modulating the microbiome, they are advancing the understanding of “how the immune response can end up out of control in autoimmunity” and that they could use this information to find “early interventions”.
inflammation in multiple sclerosis
Multiple sclerosis is a disease that affects nearly one million people in the United States. Among its most common symptoms are muscle spasmsstiffness, weakness, difficulty in movement, depression or pain.
There is currently no cure for this disease, so its treatments focus on helping patients manage their symptomscontrol outbreaks and slow the progression of the disease.
Scientists are investigating the causes of MS but no clear conclusion has yet been reached, although recent research suggests that the gut microbiome plays an important role.
The new UVA findings confirm this theory by determining that a regulator of the immune system that is found in “barrier tissues” as the intestine plays a vital role in disease. According to the researchers, this regulator can reprogram the gut microbiome to favor damaging chronic inflammation.
In the UVA research, Gaultier and his colleagues blocked the activity of the regulator, called the “aryl hydrocarbon receptor,” in a few 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 laboratory mice. With this receiver out of service, the inflammation subsided and the mice recovered.
The findings suggest that clinicians may one day take a similar approach to disrupt damaging inflammation in people with MS, although that will require much more research. Before that happens, scientists will need a much better understanding of the interactions between the immune system and the microbiome, the UVA researchers say.
Ultimately, however, the new UVA research lays a important foundation for future efforts targeting the microbiome in order to reduce the inflammation responsible for multiple sclerosis and other autoimmune diseases.
“Ultimately, honing the immune response using the microbiome could spare patients the harsh side effects of immunosuppressive drugs,” says Merchak.