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The microbiome has gained major attention in Multiple sclerosis (MS)
The therapeutic activity of interferon-beta may in part be associated with upregulation of short-chain fatty acid transporters. Distinct microbial networks were observed in untreated Multiple sclerosis (MS) and healthy controls. These results strongly support specific gut microbiome associations with Multiple sclerosis (MS) risk, course and progression, and functional changes in response to treatment
People with multiple sclerosis have been shown to have an altered microbiome, increased intestinal permeability and changes in bile acid metabolism
In a mouse model of multiple sclerosis, the gut microbiota is a significant contributor to pathology
Manipulation / Modulation of Gut microbiota may provide therapeutic targets for extraintestinal inflammatory diseases such as Multiple sclerosis (MS)
Serum analyses of Zonula Occludens-1 (ZO-1) and claudins show impaired barrier integrity in Multiple sclerosis (MS)
The mucus layer was weakened in Multiple sclerosis (MS). This was linked to bacteria that break down mucin, suggesting that gut bacteria play a role in weakening the barrier. The findings indicate that there is a reduced gut barrier function in MS, and this is associated with an increase in mucin-degrading bacteria.
Studies show an increased number of Mucin Degrading Bacteria in Multiple sclerosis (MS). This could affect the barrier function in MS.
Tight junction breakdown leads to an impaired epithelial barrier or "leaky" gut. Serum tight junction proteins can come from any barrier tissue, such as skin, endothelium, or gut. Thus, fecal measurements of tight junction-related proteins are crucial for targeted evaluations of gut wall epithelial integrity. Serum Zonula Occludens Protein-1 (ZO-1) was elevated in Multiple sclerosis (MS), but not in stool.
The intestinal mucus layer and the epithelium provide an important barrier against the gut microbiota. A disruption could contribute to Multiple sclerosis (MS). Studies that directly measure the integrity of the epithelial barrier using the lactulose:mannitol test have reported increased barrier permeability in a portion (20–60%) of subjects with Multiple sclerosis (MS)
The gut microbiome is altered in Multiple Sclerosis (MS). Specific bacterial species have been shown to promote pathogenic T and B cell responses while limiting Tregs leading to Central Nervous System (CNS) Autoimmunity
We observed a significantly increased proportion of Akkermansia muciniphila, Ruthenibacterium lactatiformans, Hungatella hathewayi, and Eisenbergiella tayi and decreased Faecalibacterium prausnitzii and Blautia species
Akkermansia, Butyricicoccus, and Mogibacteriaceae play unique roles in Multiple Sclerosis (MS).
A decrease in levels of Collinsella, Slackia, Adlercreutzia equolifaciens and Sutterella was found in people affected with Multiple sclerosis (MS). Increase in levels of Bilophila and Pseudomonas was also observed in Multiple sclerosis (MS) patients
Earlier findings also reported that Clostridium perfringens type B inhabits the gut in Multiple sclerosis (MS) patients who subsequently exhibit increase in the level of epsilon toxin in the body leading to neurodegeneration
Another side of Multiple sclerosis (MS) is pediatric Multiple sclerosis (MS), which has been reported to exhibit a significant difference in gut microbial diversity
Associations between the Multiple sclerosis (MS) intestinal microbiome and regulatory T cells (Tregs) have also been described. The genera Parabacteroides, which is reduced in Multiple sclerosis (MS) patients, was shown to stimulate IL-10+ Tregs
The phytate degradation pathway was over-represented in untreated Multiple sclerosis (MS), while pyruvate-producing carbohydrate metabolism pathways were significantly reduced
Microbiome composition, function, and derived metabolites also differed in response to disease-modifying treatments
In a proof-of-concept study, 143 patients with multiple sclerosis who received propionate supplementation alongside existing therapies experienced remission and an increase in functionally competent Treg cells. This was accompanied by a decrease in CD4+ Th1 Cells and Th17 cells. Although the mechanisms by which the microbiome is modulated through this supplementation remain unclear, the transcriptomic profiles of gut microbiomes from patients who responded to the treatment showed a correlation with genes that are positively associated with Treg induction. Conversely, genes that are negatively associated with Treg cell induction were suppressed, and the opposite trend was observed in patients who did not respond to the treatment.
Changes in microbiome levels were associated with altered expression of gene involved in maturation of dendritic cells, NFKB signaling, cytokine production, T-cell activation and interferon signalling pathways participating in neuroinflammation and disease progression
Kadowaki et al. showed that the C-C Chemokine Receptor Type 9 (CCR9) level was reduced in gut-associated lymphoid tissues in secondary progression Multiple sclerosis (MS) (SPMS) patients. In altered gut microbiome conditions, reduction in CCR9+ cells, which express transcription factor c-Maf in high levels, result in increase in retinoic acid-related orphan receptor gamma t (RORγt) expression and pro-inflammatory cytokine IL-17/interferon-γ (IFN gamma)
For example, Multiple sclerosis (MS) is characterized by inflammation and axonal damage, leading to progressive disability due to neurodegeneration. Increasing evidence suggests that microbiota plays a crucial role in the development of the disease.
A human study showed that half of the patients with multiple sclerosis exhibited enhanced TLR-2 sensitivity
see also:
Akkermansia muciniphila
Diseases / Disorders (extraintestinal manifestations)
Dysbiosis & Multiple sclerosis (MS)
Experimental Autoimmune Encephalomyelitis (EAE) & Short-Chain Fatty Acids (SCFAs)
Gut microbiota & Neurodegeneration / Neurodegenerative Diseases (NDDs)
Multiple sclerosis (MS)
Parabacteroides distasonis