Reprogram the microbiome. Found a new way to fight autoimmune diseases

Researchers from the University of Virginia have found a unique chemical regulator that triggers inflammatory responses in autoimmune diseases. By blocking it, the scientists were able to stop the inflammation.

Like many autoimmune diseases, chronic inflammation is linked to the development of multiple sclerosis, a condition that damages the sheaths around nerves, leading to muscle weakness and spasms, difficulty walking or moving, stiffness, pain, and more.

While current methods of fighting the disease focus on managing symptoms, researchers from the University of Virginia were interested in whether it was possible to turn off the mechanism that causes inflammation at its source. So, they examined the microbes inside the guts of mice and found a chemical regulator that leads to the inflammatory cascade. They also figured out how to disable it, writes New Atlas .

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Scientists are increasingly discovering how the gut microbiome can affect more than just digestive health. Just last year, we saw studies linking the colony of bacteria living in our gut to depression, exercise motivation, weight gain, rheumatoid arthritis, and excessive alcohol consumption. And earlier this year, there were reports of how the gut microbiota might influence diseases like Alzheimer’s and possibly diabetes. So it made sense that when researchers wanted to find a way to interrupt the inflammatory response that leads to multiple sclerosis, they turned to the microbiome.

Using mice, they found that a chemical regulator found in the intestinal wall can direct gut bacteria to produce inflammatory compounds. The regulator is called the aryl hydrocarbon receptor, and it is produced by T cells (a type of white blood cell that fights off invaders in the body, including allergens, disease, and cancer). Interestingly, the researchers investigated the impact regulatory T cells called Tregs could have on multiple sclerosis in 2021 and found that inhibiting a protein called Piezo1 could allow the cells to reduce inflammation in mouse models.

However, this time the research was directed at the inflammation-causing receptor. When the researchers blocked it in the guts of mice, they found that the microbiome was able to produce compounds such as bile salts and short-chain fatty acids that make it difficult for T cells to develop. As a result, inflammation was dramatically reduced, to the point where the mice were effectively cured of their disease.

The scientists note that more research will be needed to see if the results apply to humans. But the current research at least paves the way for future research that could treat multiple sclerosis differently.

“We are approaching the search for treatments for multiple sclerosis from a new direction,” said Andrea Merchak, a postdoctoral fellow in neuroscience at California State University and lead author of the study. “By modeling the microbiome, we are getting closer to understanding how the immune response can get out of control in autoimmunity. We can use this information to find early interventions.”

Merchak also said that directly targeting a specific receptor with drugs may be a more effective way to boost inflammation-fighting activity in the gut than using interventions such as probiotics or drugs that interfere with the immune system in MS patients.

“Due to the complexity of the gut flora, probiotics are difficult to use in clinical practice,” she said. This receptor can be easily targeted with drugs, so we may have found a more reliable way to maintain a healthy gut microbiome. Ultimately, fine-tuning the immune response using the microbiome could save patients from the severe side effects of immunosuppressive drugs.”

As research continues, there is hope that the discovery could lead to new treatments for other autoimmune diseases.

Previously , Focus wrote about how scientists managed to cure a girl with a complex rare autoimmune disease . The doctors deviated from the medical protocol and this helped save the life of a girl who had already been given up

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