A new breakthrough could end the chronic inflammation responsible for Multiple Sclerosis (MS).
Research has identified a vital contributor to the hyperactive autoimmune response and neuroinflammation that are the hallmarks of MS.
Blocking this lynchpin in a research model of MS alleviated the harmful inflammation, the UVA Health study revealed, giving researchers a prime target in their efforts to develop new treatments for MS and other autoimmune diseases.
Scientists have struggled to understand the causes of MS, but recent research suggests an important role for the gut microbiome.
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.
“We are approaching the search for multiple sclerosis therapeutics from a new direction,” Andrea Merchak, doctoral candidate in neuroscience, said.
“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 over 130,000 people in the UK – and around a million in the United States – with thousands more cases diagnosed globally every year.
Symptoms can include muscle spasms, stiffness, weakness, difficulty moving, depression and pain. There is no cure, so treatments focus on helping patients manage their symptoms, control flare-ups and slow the progression of the disease.
In the research, the team 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 findings suggest that doctors may one day be able to take a similar approach to interrupt the harmful inflammation in people with MS, although that will take much more research.
Before that can happen, scientists will need a much better understanding of the interactions between the immune system and the microbiome, the UVA researchers say.
Ultimately, say the researchers, UVA’s new research lays an important foundation for future efforts to target the microbiome to reduce the inflammation responsible for MS and other autoimmune diseases.
“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.”
