Looking at post-mortem brain samples, researchers found that multiple sclerosis is associated with an abundance of bacteria and molecular diversity.
Bacterial abundance and molecular diversity were linked to both neuropathology and pro-inflammatory gene expression in patients with multiple sclerosis (MS), according to new study findings.
Researchers from the University of Alberta in Canada examined the composition and abundance of microbiota in frozen and fixed autopsied brain samples from MS patients in order to identify which microbial communities resided in the tissues.
The investigators compared these samples to age and sex matched control subjects without MS and used neuropathological, molecular and bioinformatics tools.
The brain samples were obtained from MS patients with either the relapsing remitting or the progressive subtypes of MS. The researchers used stains to visualize myelin and serial brain sections were immuno labeled with antibodies to bacterial and host proteins.
The study authors wrote that bacterial genomes and proteins are present in the brains of all kinds of animals, including primates, rodents and other species in addition to humans. These microbiota communities can often be interrupted during disease, they explained.
Proteobacteria was the dominant phylum discovered in the cerebral white matter in the brains of MS patients, compared to the non MS patients, the researchers explained. The team also determined that the predominance of Proteobacteria in progressive MS patients’ white matter was linked to the increased inflammatory gene expression compared to a wider range of bacterial phyla in other relapsing remitting MS patients’ white matter.
The researchers found through RNA sequencing that there was reduced molecular diversity in MS brains, which could imply an overgrowth of select bacteria. They purport that this could be Proteobacteria, which they learned from sequencing data from progressive MS patients, though it was different from relapsing remitting MS patients on disease modifying therapeutic treatments. The researchers added that this result suggests that changes in the microbial populations in other diseased organs could be resolved by increasing microbial diversity.
The researchers concluded that the inflammatory demyelination is linked to an organ specific dysbiosis in MS that could contribute to underlying disease mechanisms. Additionally, the investigators added that the presence of bacteria in the brain and the type of bacteria present were associated with the host immune gene expression.
In a previous study, the same team transmitted human brain derived bacteria into immunocompromised mice and learned that these organisms are not viable. But, they said, being able to identify bacterial species and their impact on inflammatory demyelination could produce insights into MS prevention and treatment in the future.
Overall, the study authors wrote that further research is needed into the individual bacterial species present in brains as well as other organs that can contribute to neurological disease or health.
These types of studies are warranted, they added, because their findings could offer new therapeutic approaches or targets for inflammatory degenerative neurological diseases.
The study, “Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis,” was published in Scientific Reports.