Multiple sclerosis affects millions of people worldwide, though its underlying causes, and the physiological factors that trigger it remain unclear. Recently, however, researchers are looking to the human gut microbiota for answers.
In multiple sclerosis (MS), the immune system attacks myelin, the coating that surrounds the axons that connect nerve cells.
This damage eventually leads to symptoms, such as muscle weakness, fatigue, and vision problems. While it remains unclear what causes MS, over the past few years, researchers have been hypothesizing that gut bacteria may play a key role.
The link between the brain and the gut does not stop at mood disorders, however. Studies have linked the composition of gut microbiota with Parkinson’s disease and, more recently, researchers have suggested that it may also be involved in the development of MS.
Now, a study conducted by scientists from the University of Zürich in Switzerland indicates that the gut may trigger the harmful immune response that causes demyelination (the deterioration of myelin).
The team’s findings appear in the journal Science Translational Medicine.
Previous research from the University of Zürich team — which we covered on Medical News Today — looked at how specialized immune cells, T cells, and B cells, communicate with each other to set off demyelination.
In the current study, the scientists identified other pathways of T cell activation, noting that a protein produced by certain gut bacteria can activate these cells.
T cells, the study authors explain, react to GDP-L-fucose synthase, which is a protein produced by certain bacteria in the intestines of people with MS.
“We believe that the immune cells are activated in the intestine and then migrate to the brain, where they cause an inflammatory cascade when they come across the human variant of their target antigen.”
Study author Mireia Sospedra
More specifically, in one particular group of people with MS — those with the HLA-DRB3* genetic variation — the gut microbiota appeared to play a considerably greater role in triggering the harmful MS mechanism than previously suspected.
In the future, Sospedra and team plan to conduct further tests to assess GDP-L-fucose synthase’s interaction with immune cells.
The researchers’ chief goal is to come up with a better, more focused and effective treatment for MS.
Existing approaches target the whole immune system, which means that, while this may counteract harmful MS mechanisms, it also weakens helpful immune responses.
However, “our clinical approach specifically targets the pathological autoreactive immune cells,” notes Sospedra. In other words, the scientists from the University of Zurich aim to act on the specific “rogue” immune cells that attack myelin.
The aim is to collect blood samples from people diagnosed with MS and then attach relevant components of GDP-L-fucose synthase to red blood cells in the laboratory.
When reinjected into the person’s bloodstream, this modified blood should allow the immune system to “learn” not to attack myelin.
Importantly, by targeting specific cells, rather than the entire immune system, the scientists hope to eliminate potentially serious side effects.