Gut Microbiome Interactions in Autoimmune Ocular Diseases

The gut microbiome exerts a profound influence on autoimmune disorders affecting the eye through a network of immunological and metabolic pathways. Alterations in microbial composition, or dysbiosis, can compromise intestinal barrier integrity, promote systemic inflammation and reshape T-cell responses. In experimental models of autoimmune uveitis, shifts in commensal communities precede activation of retina-specific T cells in gut-associated lymphoid tissue. Loss of short-chain fatty acid–producing bacteria diminishes regulatory T-cell induction, allowing effector T cells to migrate to the eye and precipitate inflammation. In Sjögren’s syndrome, reduced diversity of gut and mucosal microbiota correlates with severity of dry-eye manifestations, implicating microbial signals in lacrimal gland dysfunction. Similar patterns are emerging in Behçet’s disease, where enrichment of sulphate-reducing and opportunistic genera coincides with enhanced ocular inflammation. Together, these findings define a gut–eye axis in which microbial metabolites, barrier function and immune priming interconnect, offering novel targets for therapeutic intervention and personalised management of autoimmune ocular disease.

Research from Nature Portfolio

Experimental administration of propionate and other short-chain fatty acids in a mouse model of autoimmune uveitis has been shown to attenuate ocular inflammation by expanding regulatory T cells in intestinal lamina propria and cervical lymph nodes, while suppressing effector T-cell induction and trafficking to the eye. In Sjögren’s syndrome, analysis of patient and mouse microbiomes reveals a marked reduction in commensal Clostridium and Faecalibacterium alongside increased Enterobacter and Pseudomonas. Lower microbial diversity and diminished butyrate producers correlate with more severe ocular surface disease, suggesting that restoration of specific microbial taxa may alleviate dry-eye pathology.

Gut Microbiome Interactions in Autoimmune Ocular Diseases publication trend

The graph below shows the total number of articles in gut microbiome interactions in autoimmune ocular diseases across all publications each year (not limited to Nature Index journals).

Technical terms

Gut–eye axis: Bidirectional communication between the intestinal microbiota and ocular immune and physiological processes.

Dysbiosis: A pathological imbalance in the composition or function of the gut microbiome.

Short-chain fatty acids (SCFAs): Microbial fermentation products of dietary fibre that regulate host immunity and barrier integrity.

Regulatory T cells: A subset of T lymphocytes that enforce immune tolerance and suppress autoreactive responses.

Faecal microbiota transplantation (FMT): Transfer of stool from a healthy donor to restore microbial diversity and function in a recipient.

Molecular mimicry: Similarity between microbial antigens and host proteins that may precipitate autoimmunity.

References

1. Altered Mucosal Microbiome Diversity and Disease Severity in Sjögren Syndrome. Scientific Reports (2016).
2. Short chain fatty acids ameliorate immune-mediated uveitis partially by altering migration of lymphocytes from the intestine. Scientific Reports (2017).
3. Microbiome and Autoimmune Uveitis. Frontiers in Immunology (2019).
4. A metagenomic study of the gut microbiome in Behcet’s disease. Microbiome (2018).
5. Targeting the Gut–Eye Axis: An Emerging Strategy to Face Ocular Diseases. International Journal of Molecular Sciences (2023).