A new study shows that not only the composition of the intestinal flora plays a role in multiple sclerosis, but that specific myelinlike surface structures on certain bacteria could also contribute to the initiation and progression of the disease. Moreover, it provides valuable insights into the potential of microbiome-based treatments in MS

When the immune system confuses friend and foe, autoimmune diseases develop. In the case of MS, it mistakenly attacks the body’s protective layer of nerve fibers, known as the myelin sheath. Those affected can experience exhaustion and numbness in their limbs, develop walking problems and may even become paralyzed.

If gut bacteria are too similar to the protective layer of nerves, they can misdirect the immune system and cause it to attack its own nervous system. This mechanism can accelerate the progression of MS. Scientists have spent decades investigating the question of how this fatal error in our defenses occurs. More recent hypotheses focus on the intestinal flora. This is because people with MS have a different composition of microorganisms in their intestines than healthy people.

One theory suggests proinflammatory gut bacteria, which have similar surface structures to the myelin sheath of the nerves, upset the immune system. The immune cells then attack both the harmful bacteria and the body’s own myelin sheath. Experts refer to this likeness between bacteria and myelin sheath as “molecular mimicry.”

Using molecular biological methods, researchers at the University of Basel modified proinflammatory Salmonella bacteria so they had a surface structure similar to that of the myelin sheath. They used bacteria of the same species without a self-structure as controls.

In genetically modified mice, which can serve as a disease model for MS, the myelin-like Salmonella bacteria caused a markedly faster progression of the disease than the control bacteria. According to the researchers, the proinflammatory bacteria alone only fuel the disease to a limited extent. But the combination of an inflammatory environment and molecular mimicry activates specific immune cells. These multiply, migrate into the nervous system, and attack the myelin sheath there.
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The research team conducted the same trials with E. coli bacteria, which are part of the normal intestinal flora and are noninflammatory. When they implanted the myelin-like E. coli bacteria into the mice, the progression of the disease was milder.

The study shows that not only the composition of the intestinal flora plays a role in MS, but that specific myelin-like surface structures on certain bacteria could contribute to the initiation and progression of the disease. It also provides valuable insights into the potential of microbiome-based treatments in MS. These could train the immune system with the help of specifically modified bacteria, so it no longer targets the myelin sheath.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. The researchers said the results call for caution because some cancer treatments use the microbiome to stimulate the immune system to combat the tumor. This may also create an environment in the intestine in which molecular mimicry can trigger autoimmune reactions or even diseases.

The study was published in the journal Gut Microbes.