CHARLOTTESVILLE, Va. (CBS19 NEWS) -- People who have been diagnosed with the autoimmune disease multiple sclerosis know the struggle against the inflammation that causes its symptoms.

But neuroscientists at the University of Virginia Health System say they have found a potential way to disrupt that chronic inflammation.

According to a release, the new study has identified a vital contributor to the hyperactive autoimmune response and neuroinflammation that are the hallmarks of MS.

By blocking this contributor, called the “aryl hydrocarbon receptor” in certain immune cells, in a research model, the scientists found a target on which to focus their efforts to develop new treatments for MS and other autoimmune diseases.

“We are approaching the search for multiple sclerosis therapeutics from a new direction,” said Andrea Merchak, a doctoral candidate in neuroscience and researcher in the lab of Alban Gaultier, PhD. “By modulating the microbiome [the collection of microorganisms that naturally live inside us], we are making inroads in understanding how the immune response can end up out of control in autoimmunity. We can use this information to find early interventions.”

MS affects nearly a million Americans, with symptoms ranging from muscle spasms to stiffness to difficulty moving to pain and weakness among others.

At this time, there is no cure for the condition, so existing treatments are focused on helping patients manage the symptoms they experience, control flare-ups, and slow the progression of the disease.

In the past, scientists had struggled to understand what caused MS, but recent research has suggested that the gut microbiome plays an important role.

The release says these new findings bolster that suggestion, showing that an immune system controller found in “barrier tissues” such as the intestine has vital roles in the condition.

This regulator seems to have the ability to reprogram the gut microbiome to promote harmful, chronic inflammation.

The researchers blocked the activity of the regulator in immune cells called T cells and found it had a dramatic impact on the production of bile acids and other metabolites in the microbiomes of lab mice.

When the receptor was put out of commission, the inflammation the mice experienced decreased and they recovered.

The release says these findings suggest that doctors may someday be able to take a similar approach to interrupt harmful inflammation in people with MS.

However, scientists say they need a better understanding of the interactions between the immune system and the microbiome before that can happen.

Still, they believe this research lays a foundation for future efforts to target the microbiome and reduce inflammation.

This project is part of the UVA TransUniversity Microbiome Initiative, a central hub for the university’s research into the microbiome.

These findings have been published in the scientific journal PLOS Biology.