Finding that could end the chronic inflammation of multiple sclerosis
Neuroscientists at the University of Virginia Health System (UVA). in the USA have discovered a potential way to disrupt the chronic inflammation responsible for multiple sclerosis (MS).
The new UVA study identifies an essential factor in the overactive autoimmune response and the neuroinflammation which are hallmarks of MS. Blocking this axis in an MS research model alleviated harmful inflammation, providing researchers with a prime target in their efforts to develop new treatments for multiple sclerosis and other autoimmune diseases.
The research was conducted by. Andrea MerchakD. candidate in neuroscience, and her colleagues in the laboratory of Dr. Alban Gaultier, Ph.D., of the Department of Neuroscience at the University of Virginia School of Medicine and its Brain and Glia Immunology (BIG) Center.
“We are approaching the search for therapies for multiple sclerosis from a new direction,” says Merchak. The researcher also explains that by modulating the microbiome they advance 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 the muscle spasmsstiffness, weakness, difficulty of movement, depression or pain.
There is currently no cure for this disease, so its treatments focus on helping patients manage their symptoms., control flare-ups and slow the progression of the disease.
Scientists investigate the causes of MS but no clear conclusion has yet been reached although recent research suggests that the gut microbiome plays an important role.
New UVA findings confirm this theory by determining that a regulator of the immune system that is found in “barrier tissues” such as the gut plays a vital role in disease. According to the researchers, this regulator may reprogram the intestinal microbiome to promote harmful chronic inflammation.
In the UVA research, Gaultier and his collaborators blocked the activity of the regulator, termed the “aryl hydrocarbon receptor,” in some 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 receptor out of commission, inflammation decreased and the mice recovered.
The findings suggest that clinicians may someday take a similar approach to disrupting harmful 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, say the UVA researchers.
Ultimately, however, the new UVA research sets a important foundation for future efforts directed at the microbiome. in order to reduce the inflammation responsible for multiple sclerosis and other autoimmune diseases.
“Ultimately, fine-tuning the immune response using the microbiome could spare patients the harsh side effects of immunosuppressive drugs,” Merchak says.
