Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), characterized by inflammation, demyelination, and neuronal damage.

The exact cause of MS is still unknown, but it is believed to be a complex interplay between genetic and environmental factors. Recent studies have revealed the potential role of bacteria in the development and progression of MS. In this article, we will explore the role of bacteria in the pathogenesis of MS and their possible therapeutic implications.

Bacteria and the gut-brain axis in MS

The gut-brain axis (GBA) is a complex bidirectional communication network between the gut microbiota and the CNS.

The gut microbiota plays a critical role in the development and function of the immune system, and dysbiosis (imbalance in the gut microbiota) has been associated with several autoimmune and inflammatory diseases.

Several studies have shown alterations in the gut microbiota composition and function in MS patients.

For instance, MS patients have been found to have reduced microbial diversity and increased levels of some bacterial taxa, such as Akkermansia muciniphila and Methanobrevibacteriaceae, compared to healthy controls. Conversely, other bacterial taxa, such as Prevotella and Bacteroides, have been found to be decreased in MS patients.

Mounting evidence suggests that changes in the gut microbiota composition and function may contribute to MS pathogenesis by modulating immune responses and exacerbating CNS inflammation.

For instance, studies in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, have shown that gut dysbiosis exacerbates EAE severity by promoting pro-inflammatory immune responses.

Moreover, several studies have demonstrated a potential link between MS and gut inflammation, as MS patients have been found to have increased levels of inflammatory cytokines, such as interleukin (IL)-17 and IL-23, in the gut mucosa.

The potential role of specific bacterial species in MS pathogenesis

Recent studies have identified specific bacterial species that may play a role in MS pathogenesis by modulating immune responses and CNS inflammation. For instance, a study by Chen et al.

found that the oral microbiota of MS patients was enriched in pro-inflammatory bacterial species, such as Fusobacterium and Peptostreptococcus, compared to healthy controls. Another study by Cekanaviciute et al. demonstrated that the gut commensal bacteria Akkermansia muciniphila ameliorated EAE severity by inducing regulatory T cells (Tregs) and reducing pro-inflammatory cytokines.

Moreover, a recent study by Berer et al. demonstrated that the gut commensal bacterium segmented filamentous bacterium (SFB) induced a pro-inflammatory Th17 cell response in the gut and enhanced EAE severity in mouse models.

Additionally, the study found that germ-free mice, which lack commensal bacteria, were protected against EAE, and colonization with SFB restored EAE susceptibility.

The potential therapeutic implications of manipulating the gut microbiota in MS

The emerging evidence linking gut dysbiosis and MS pathogenesis suggests that manipulating the gut microbiota may be a potential therapeutic strategy for MS.

Several preclinical and clinical studies have investigated the potential therapeutic implications of probiotics, prebiotics, and fecal microbiota transplantation (FMT).

For instance, a pilot study by Tankou et al.

found that MS patients who consumed a probiotic yogurt containing Lactobacillus, Bifidobacterium, and Streptococcus had a significant reduction in pro-inflammatory cytokine levels and an increase in anti-inflammatory cytokine levels compared to placebo. Additionally, a randomized controlled trial by Kouchaki et al. demonstrated that supplementation with the prebiotic oligofructose-enriched inulin improved fatigue and quality of life in MS patients.

Moreover, a clinical trial by Borody et al. investigated the safety and efficacy of FMT in MS patients and found that FMT led to significant improvements in fatigue, depression, and quality of life.

Conclusion

The emerging evidence linking the gut microbiota and MS pathogenesis suggests that bacteria may play a critical role in the development and progression of MS.

Dysbiosis in the gut microbiota has been associated with alterations in immune responses and CNS inflammation, contributing to MS pathogenesis. Manipulating the gut microbiota through dietary interventions, probiotics, prebiotics, or FMT may be a potential therapeutic strategy for MS.

Further studies are needed to elucidate the exact mechanisms underlying the role of the gut microbiota in MS and to evaluate the safety and efficacy of microbiota-targeted therapies.