As you know microbiome is my favourite subject,so when this paper came out in a Top Science Comic I thought I better let you have a look as it is your new hope.
Mice were given an antibiotic cocktail that contained ampicillin, vancomycin, neomycin and metronidazole in their drinking water one week before sensitization to MOG peptide fragment 35–55 (MOG35–55), and the antibiotic treatment was continued throughout the experiment. Depletion of the gut microbiota by this antibiotic cocktail resulted in attenuated symptoms of experimental autoimmune encephalomyelitis (EAE) Notably, the treatment with ampicillin alone, but not with the other antibiotics in isolation also limited the development of EAE They track down a gut bacteria and found that another was needed that cross-reactive reacted with myelin reactive T cells. So a few rogue bacteria are the problem and antibiotics are a solution
Apparently the authors said “Our data emphasize the necessity of considering the synergistic effects of intestinal microbes on autoimmune diseases and give hope to people looking for effective treatments for multiple sclerosis.”
So should you be taking anti-biotics and this is the solution to MS, But before you start they apparently also have said
“But, because gut microbes and T cell binding locations on myelin differ between mouse and human, further studies using human microbes and autoreactive T cells are now needed.”
I suppose this is why we need to understand if its the B cells are important on not because if it is not the T cells, then the logic falls apart
Accumulating evidence indicates that gut microorganisms have a pathogenic role in autoimmune diseases, including in multiple sclerosis. Studies of experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis), as well as human studies, have implicated gut microorganisms in the development or severity of multiple sclerosis. However, it remains unclear how gut microorganisms act on the inflammation of extra-intestinal tissues such as the spinal cord. Here we show that two distinct signals from gut microorganisms coordinately activate autoreactive T cells in the small intestine that respond specifically to myelin oligodendrocyte glycoprotein (MOG). After induction of experimental autoimmune encephalomyelitis in mice, MOG-specific CD4+ T cells are observed in the small intestine. Experiments using germ-free mice that were monocolonized with microorganisms from the small intestine demonstrated that a newly isolated strain in the family Erysipelotrichaceae acts similarly to an adjuvant to enhance the responses of T helper 17 cells. Sequencing of the contents of the small intestine revealed a strain of Lactobacillus reuteri that possesses peptides that potentially mimic MOG. Mice that were co-colonized with these two strains showed experimental autoimmune encephalomyelitis symptoms that were more severe than those of germ-free or monocolonized mice. These data suggest that the synergistic effects that result from the presence of these microorganisms should be considered in the pathogenicity of multiple sclerosis, and that further study of these microorganisms may lead to preventive strategies for this disease.