Gut Microbiota Effects on Autoimmune Neuroinflammation

The human gut microbiota exerts a profound influence on autoimmune neuroinflammation through metabolic, immunological and barrier interactions. Dysbiosis alters the production of key microbial metabolites such as short-chain fatty acids, compromises epithelial and blood-brain barrier integrity, and skews the balance of pro-inflammatory and regulatory immune cells. In multiple sclerosis, shifts in taxa—including Akkermansia and Faecalibacterium—correlate with relapse activity and treatment response. Preclinical models of experimental autoimmune encephalomyelitis (EAE) have shown that microbial community networks, host-specific factors and metabolite profiles can modulate the differentiation of Th17 and regulatory T cells, influencing disease severity. The gut-brain axis—encompassing immune signalling, vagal pathways and microbial products—provides a mechanistic framework for bidirectional communication between the gut and central nervous system. Therapeutic strategies targeting diet, probiotics, prebiotics and receptor agonists hold global promise to mitigate autoimmune neuroinflammation.

Research from Nature Portfolio

Recent studies in pre-clinical models have emphasised the complexity of predicting neuroinflammatory outcomes from microbiota composition alone. One study in mice with experimental autoimmune encephalomyelitis demonstrated that neither the presence nor abundance of suspected microbial risk taxa reliably forecasted disease course. Instead, the immunoglobulin A coating index of specific bacteria before disease onset emerged as an accurate individual predictor of severity, underscoring the importance of host–microbe interactions within community networks. An earlier investigation in people with multiple sclerosis revealed distinct alterations in gut bacterial composition, including increased Methanobrevibacter and Akkermansia, and decreased Butyricimonas, which correlated with changes in immune gene expression and responses to disease-modifying therapies. These foundational findings link microbial shifts with immunological pathways and suggest biomarkers for patient stratification.

Gut Microbiota Effects on Autoimmune Neuroinflammation publication trend

The graph below shows the total number of articles in gut microbiota effects on autoimmune neuroinflammation across all publications each year (not limited to Nature Index journals).

Technical terms

Experimental autoimmune encephalomyelitis (EAE): An animal model of central nervous system autoimmunity mimicking multiple sclerosis.

Short-chain fatty acids (SCFAs): Microbial fermentation products, such as acetate, propionate and butyrate, that modulate immune responses and barrier function.

Dysbiosis: An imbalance in microbial community composition associated with disease states.

Gut-brain axis: Bidirectional network of neural, immune and metabolic signalling pathways connecting the gastrointestinal tract and central nervous system.

Th17 cells: A subset of pro-inflammatory T helper cells implicated in autoimmune pathology of the central nervous system.

References

1. Gut microbial factors predict disease severity in a mouse model of multiple sclerosis. Nature Microbiology (2024).
2. Dietary ellagic acid therapy for CNS autoimmunity: Targeting on Alloprevotella rava and propionate metabolism. Microbiome (2024).
3. The gut microbiota in multiple sclerosis varies with disease activity. Genome Medicine (2023).
4. GPR43 stimulation on TCRαβ+ intraepithelial colonic lymphocytes inhibits the recruitment of encephalitogenic T-cells into the central nervous system and attenuates the development of autoimmunity. Journal of Neuroinflammation (2023).
5. The Gut-Brain Axis: How Microbiota and Host Inflammasome Influence Brain Physiology and Pathology. Frontiers in Immunology (2020).
6. Gut microbiome of multiple sclerosis patients and paired household healthy controls reveal associations with disease risk and course. Cell (2022).