Gut Microbiome

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Article initiated by:
Eric Kim, Viren Rana, DO, Nicole Lifson MD
All contributors:
Prof. Dr. Arvind Kumar Morya MBBS, MS, MNAMS, Srishti Khullar, Priyanka P, Bhawna.Sharma, Mamta.Singh, Viren Rana, DO, Srishti Khullar, Prof. Dr. Arvind Kumar Morya MBBS, MS, MNAMS
Assigned editor:
Review:
Assigned status Update Pending
.


Introduction

The gut microbiome refers to the commensal bacteria, fungi, viruses, archaea, and their metabolites that interact with host immunity, metabolism, epithelial barrier function, and systemic inflammation.[1] Increasing evidence suggests that gut dysbiosis may influence ocular health through a “gut-eye axis,” in which microbial products, immune mediators, and metabolites affect the ocular surface, retina, uvea, optic nerve, and retinal vasculature. Although associations have been reported between gut dysbiosis and several ocular diseases, causality remains incompletely established. Most current evidence is observational or preclinical, and microbiome-targeted therapies remain investigational in ophthalmology.

The Gut-Eye Axis

  • The gut-eye axis refers to the bidirectional relationship between the intestinal microbiome and ocular health[2].
  • Gut dysbiosis may influence the eye through immune, metabolic, vascular, endocrine, and neural pathways.
  • Proposed mechanisms include altered intestinal permeability, systemic inflammation, Th17/Treg imbalance, complement activation, and changes in microbial metabolites such as short-chain fatty acids, bile acids, tryptophan metabolites, and trimethylamine-N-oxide. [3][4](Table 1)
  • These pathways may contribute to ocular surface inflammation, uveitis, retinal degeneration, retinal vascular disease, glaucoma, and other immune-mediated or degenerative eye disorders. (Figure 1)
    Figure 1: The Gut-Eye Axis

Table 1: Mechanisms linking gut dysbiosis to ocular disease

Mechanism How it may affect the eye Example ocular relevance
Immune modulation Alters T-cell homeostasis, Th17/Treg balance, cytokine tone Uveitis, Sjogren’s syndrome, dry eye
Barrier dysfunction Increased intestinal permeability and endotoxemia may promote systemic inflammation Ocular surface inflammation, retinal vascular disease
Microbial metabolites SCFAs, bile acids, tryptophan metabolites and TMAO influence inflammatory and vascular pathways AMD, diabetic retinopathy, dry eye, RAO
Complement activation Microbiome-related inflammation may interact with complement pathways AMD
Vascular/metabolic signaling TMAO, lipid pathways, oxidative stress and endothelial dysfunction RAO, diabetic retinopathy
Neuroinflammation Immune-metabolic signaling may influence retina and optic nerve vulnerability Glaucoma, neuro-ophthalmic associations

Composition of the Gut Microbiome

  • The gut microbiome is a complex ecosystem composed of bacteria, fungi, viruses, archaea, and their metabolic products.
  • Bacteria are the dominant component, with Firmicutes and Bacteroidetes representing the major phyla, while Actinobacteria, Proteobacteria, and Verrucomicrobia are also important contributors.
  • In addition to bacteria, the gut contains a mycobiome made up of fungi such as Candida, Saccharomyces, and Malassezia, as well as a virome composed largely of bacteriophages that influence bacterial ecology.[5](Table 2)
  • From an ophthalmic perspective, the functional output of the microbiome may be more important than the presence of any single organism.
  • Microbial metabolites such as short-chain fatty acids, bile acids, tryptophan metabolites, lipopolysaccharide, and trimethylamine-N-oxide may influence immune regulation, epithelial barrier integrity, systemic inflammation, vascular function, and retinal or ocular surface homeostasis.[4][6]
  • Therefore, studies of the gut-eye axis increasingly focus not only on microbial composition, but also on microbial diversity, dysbiosis, metabolite profiles, and host immune response.

Table 2. Components of the gut microbiome and ocular relevance

Component Most commonly noted examples Ocular relevance
Bacteria Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria SCFA production, barrier function, immune regulation
Viruses/virome Primarily bacteriophages Influence bacterial ecology and microbial stability
Fungi/mycobiome Candida, Saccharomyces, Malassezia, Cladosporium May influence ocular inflammatory diseases including uveitis
Archaea Methanogenic species in some individuals May influence microbial metabolism; evidence in ocular disease remains limited
Metabolites SCFAs, bile acids, tryptophan metabolites, TMAO Functional link between gut microbiota and ocular inflammation/vascular disease

Factors that Affect the Diversity of the Microbiome

  • Gut microbiome diversity is dynamic and varies between individuals according to age, diet, geography, genetics, medications, lifestyle, environmental exposures, and systemic disease.
  • Early-life factors such as mode of delivery, breastfeeding, antibiotic exposure, and childhood diet influence initial microbial colonization, while adult microbial composition is strongly shaped by diet, medications, metabolic disease, immune status, physical activity, stress, sleep, and aging.[7]
  • These factors are important in gut-eye axis research because many ocular diseases, such as age-related macular degeneration, diabetic retinopathy, glaucoma, uveitis, and dry eye disease, occur in populations where age, systemic comorbidities, medication use, and diet may independently alter the microbiome.(Table 3)
  • Interpretation of microbiome studies is also affected by technical factors, including stool collection method, sequencing platform, bioinformatic pipeline, definition of microbial diversity, and whether studies analyze microbial composition, functional pathways, or metabolites.
  • Therefore, differences in microbiome diversity should be interpreted cautiously, as they may reflect confounding by diet, geography, drugs, systemic disease, or methodology rather than a direct causal relationship with ocular disease.[8]


Table 3. Factors Influencing Gut Microbiome Diversity

Factor Effect on microbiome Clinical Relevance
Age Changes diversity and immune-metabolic tone Major confounder in AMD and glaucoma
Diet Fiber and plant-rich diets promote SCFA-producing organisms May alter inflammatory phenotype
Antibiotics Reduce diversity and alter taxa Major confounder in all microbiome studies
Proton pump inhibitors Alter gastric and intestinal microbial composition Common in elderly patients
Diabetes/metabolic syndrome Associated with dysbiosis and vascular inflammation Confounds DR and AMD associations
Geography/ethnicity Changes baseline microbiome composition Limits generalizability of findings
Immunosuppression Modifies bacterial/fungal communities Important in uveitis and autoimmune disease
Sequencing/bioinformatics method Affects reported taxa and diversity metrics Explains heterogeneity across studies

Dysbiosis and Ocular Disease : Association versus Causation

  • Dysbiosis refers to an alteration in the composition, diversity, or functional output of the microbiome.
  • In ocular disease, dysbiosis has been associated with inflammatory, vascular, degenerative, and ocular surface disorders. However, association does not prove causation.
  • Dysbiosis may contribute to disease pathogenesis, occur secondary to systemic inflammation, reflect medication or dietary changes, or represent a biomarker rather than a direct therapeutic target.

Ocular Diseases Associated with Gut Dysbiosis

  • Gut dysbiosis has been associated with several ocular diseases, particularly inflammatory, degenerative, vascular, and ocular surface disorders.
  • The strongest biologic connection exists for diseases in which systemic immune activation, mucosal dysregulation, oxidative stress, endothelial dysfunction, complement activation, or microbial metabolites may influence ocular tissues.[9][10](Table 4)
  • Reported associations include dry eye disease, Sjögren’s syndrome, uveitis, age-related macular degeneration, diabetic retinopathy, glaucoma, retinal vascular disease, keratitis, and retinopathy of prematurity.(Table 5)
  • However, most human data remain observational, and dysbiosis may act as a contributor, biomarker, disease consequence, or confounder rather than a direct cause.

Table 4. Disease-level summary of gut microbiome associations

Ocular disease Strength of evidence Proposed mechanism Clinical implication
Uveitis Moderate: human observational + experimental support Immune dysregulation, Th17/Treg imbalance, microbial metabolites Potential future microbiome-targeted therapy; not standard care
Age-related macular degeneration Moderate observational evidence Complement activation, oxidative stress, lipid metabolism Possible biomarker/therapeutic target
Dry eye/Sjogren’s syndrome Moderate for association; mechanisms plausible Mucosal immune dysregulation, barrier dysfunction, SCFA changes Potential probiotic/diet trials; routine testing not advised
Diabetic retinopathy Emerging Metabolic inflammation, endothelial dysfunction, microglial activation May modify risk/progression; clinical role uncertain
Retinopathy of prematurity Limited but plausible Neonatal gut development, VEGF signaling, angiogenesis Future predictive biomarker; early evidence
Retinal artery occlusion Limited TMAO/lipid metabolism and vascular inflammation Vascular risk link; not diagnostic
Keratitis Limited/emerging Systemic immune tone and dysbiosis Research-level association; local risk factors dominate
Glaucoma Emerging human and experimental evidence immune activation, neuroinflammation, vascular/metabolic signaling investigational
Idiopathic intracranial hypertension limited human observational evidence obesity-metabolic axis, neurovascular regulation, medication-microbiome interaction investigational
Myopia early observational evidence dopamine/GABA-linked taxa, metabolic signaling not clinically actionable
Keratitis limited gut + ocular microbiome evidence immune modulation, altered commensals, bacterial-fungal networks local risk factors remain dominant

Table 5. Selected microbial changes reported in ocular disease

Disease Reported increase Reported decrease Interpretation
AMD Prevotella, Anaerotruncus, Oscillibacter Ruminococcaceae Observational association; not diagnostic
Uveitis Prevotella, Streptococcus, selected fungal taxa Faecalibacterium, Ruminococcus, Lachnospiraceae, Bacteroides Inflammatory phenotype; mechanisms plausible
POAG Prevotellaceae, Enterobacteriaceae, Escherichia coli Megamonas, Bacteroides plebeius Early evidence with heterogeneity
DR Variable changes; dysbiosis in some cohorts Bacteroidetes/Actinobacteria reductions in some studies Confounded by diabetes/metabolic status
ROP Enterobacteriaceae enrichment in some infants Protective amino acid metabolism pathways in controls Neonatal angiogenesis hypothesis
Keratitis Pro-inflammatory bacterial/fungal taxa reported SCFA-producing taxa reduced in some studies Limited evidence; not clinically actionable
Dry eye/Sjogren’s Variable: Proteobacteria, Actinobacteria, Bacteroidetes in some studies SCFA-producing bacteria in some studies Study heterogeneity; subtype matters

Gut Microbiome and Negative Associations with Human Health

  • Dysbiosis of the gut microbiome can manifest in a variety of ways, including diarrhea, nausea, and acid reflux.[7]
  • In addition, BMI, weight, and blood pressure have also been shown to have a significant negative correlation with diversity.[7]
  • A dysbiotic microbiome has been associated with a variety of diseases. For example, those with lung cancer exhibit reduced Actinobacteria abundance.[11]
  • There is growing evidence that dysbiosis of the gut microbiome also plays a role in various inflammatory bowel conditions, such as Crohn’s disease and ulcerative colitis.[12] However, to date, it is still unclear whether dysbiosis is a direct cause of inflammatory bowel syndrome or if dysbiosis occurs secondarily.[12]
  • Dysbiosis has been linked to celiac disease, multiple sclerosis, rheumatoid arthritis, type 1 diabetes, colorectal cancer, and systemic lupus erythematosus.[12][13][14]

Ocular Pathologies Associated with Gut Microbiome Dysbiosis

Ocular Surface Disease, Dry Eye, and Sjogren’s Syndrome

  • The gut microbiome may influence ocular surface homeostasis through mucosal immune regulation, systemic inflammatory signalling, and epithelial barrier function.[15]
  • Dysbiosis has been reported in dry eye disease and Sjogren’s syndrome, although reported microbial signatures vary across studies.
  • This heterogeneity likely reflects differences in patient selection, systemic autoimmune activity, diet, medications, sequencing methods, and dry eye subtype.
  • At present, microbiome testing is not part of routine dry eye evaluation.
  • Microbiome-directed interventions remain investigational and should not replace established dry eye or Sjogren’s syndrome management.[16][17]

Uveitis and Immune-Mediated Ocular Inflammation

  • Uveitis is one of the most biologically plausible ocular conditions linked to gut dysbiosis because systemic immunity and mucosal immune regulation are central to disease pathogenesis.
  • Studies have reported altered bacterial and fungal diversity in uveitis, including changes in short-chain-fatty-acid-producing bacteria and enrichment of potentially pro-inflammatory taxa.[18](Table 6)
  • Proposed mechanisms include altered intestinal permeability, Th17/Treg imbalance, molecular mimicry, systemic immune activation, and changes in microbial metabolites.[19][20]

Table 6. Uveitis-related microbiome associations

Disease Microbiome finding Proposed relevance
Noninfectious uveitis Reduced SCFA-producing bacteria; increased pro-inflammatory taxa Systemic immune activation
VKH disease Altered enterotypes and lactate-producing bacteria reported Potential immune modulation
Behcet disease Reduced butyrate producers; increased sulfate-reducing bacteria in some studies Inflammatory gut-immune axis
Experimental autoimmune uveitis Microbiome manipulation may modify inflammation Supports mechanistic plausibility

Retinal and Vascular Disease

  • Retinal diseases may be influenced by gut microbiome-derived immune, metabolic, complement, and vascular pathways.[21]
  • Dysbiosis has been associated with age-related macular degeneration, diabetic retinopathy, retinal artery occlusion, and retinopathy of prematurity, although causality and clinical applicability remain under investigation.[22][23](Table 7)

Table 7: Retinal diseases and proposed gut-eye mechanism

Retinal disease Proposed gut-eye mechanism Current clinical status
AMD Complement activation, oxidative stress, lipid metabolism Observational; biomarker potential
Diabetic retinopathy Metabolic inflammation, endothelial dysfunction, microglial activation Emerging evidence
Retinal artery occlusion TMAO/lipid metabolism and vascular inflammation Limited evidence
ROP Neonatal gut development, VEGF signaling, angiogenesis Early evidence

Idiopathic intracranial hypertension

  • Idiopathic intracranial hypertension(IIH) has been linked to gut dysbiosis because of its association with obesity and metabolic dysfunction.[24]
  • Research showed that patients with idiopathic intracranial hypertension who received acetazolamide had increased amounts of lactobacillus, indicating that gut dysbiosis might play a role as both an immuno-metabolic and neurovascular modulator.[6]
  • At present, there is no established clinical role of gut microbiome in evaluation or management of IIH.

Myopia

  • Prevotella copri is predominant in several studies comparing patients with stable myopia to those with progressive myopia.[6]
  • Dopamine signaling plays a known role in the development of experimental myopia, while specific bacterial taxa are also found in greater abundance in these cases. However, no microbiome-based therapies have been validated for the prevention or treatment of myopia.[25]

Glaucoma

  • Gut dysbiosis has been linked to glaucoma as per few experimental human studies but findings are currently hypothesis-generating and should not be used for routine diagnosis, risk stratification, or treatment.[26][27][28][29]

Grave's Disease

A recent study found that people with both Graves’ disease and Graves’ orbitopathy have significantly lower serum levels of indolepropionic acid, indole-3-lactate, and indoleacetic acid (IAA), identifying IAA as a possible biomarker for Graves’ orbitopathy progression. Other research linked Veillonella and Megamonas species to thyroid-associated ophthalmopathy symptoms and showed that Klebsiella pneumoniae correlates with more severe disease.[6]

Chalazion

Two studies have evaluated probiotic therapy for chalazion. The pediatric trial demonstrated accelerated lesion resolution, whereas the adult trial observed benefits limited to smaller chalazia, with no significant impact on larger lesions.[6]

Infectious keratitis

  • Alterations in gut bacterial and fungal communities have been reported in fungal and bacterial keratitis.[30]
  • Proposed mechanisms include systemic immune modulation, altered inflammatory tone, and changes in protective commensal organisms. [31]
  • However, the clinical relevance of gut dysbiosis in infectious keratitis remains uncertain because local ocular surface factors, trauma, contact lens use, agricultural exposure, antimicrobial treatment, and corneal microbiota are major determinants of disease risk and severity.

Microbiome-Targeted Interventions: Current status

  • Microbiome-targeted therapy for ocular disease remains investigational.
  • General measures that support gut microbial health, such as balanced dietary pattrns rich in fiber and plant-based foods, may have systemic health benefits, but they should not be presented as proven treatment for ocular disease.
  • Probiotics, prebiotics, synbiotics, antibiotics, and fecal microbiota transplantation are being studied as potential strategies to modify gut dysbiosis. However, probiotic effects are strain-specific, disease-specific, and influenced by host factors. [32] (Table 8)
  • Fecal transplants may also be a promising avenue for treating gut dysbiosis and associated ocular manifestations. A study by Wang et al. found that germ-free mice exhibited greater disruption of the barrier, a significant loss of goblet cells, and increased infiltration of inflammatory cells within the lacrimal gland. However, when these germ-free mice were given fecal microbiota transplants (FMT) from healthy mice, their ocular symptoms improved.[33]
  • At present, no microbiome-directed therapy should replace standard ophthalmic treatment for AMD, uveitis, glaucoma, dry eye, keratitis, diabetic retinopathy, or ROP.(Table 9).

Table 8: Microbiome-targeted interventions: current status

Intervention Potential role Current limitation
Diet/fiber Supports SCFA-producing bacteria Not disease-specific therapy
Prebiotics Promote beneficial microbial growth Optimal type and dose unknown
Probiotics May modulate immune response Strain-specific evidence; limited ocular trials
Synbiotics Combined prebiotic plus probiotic strategy Limited ocular evidence
Antibiotics May alter dysbiosis in experimental settings Risk of worsening dysbiosis and antimicrobial resistance
Fecal Microbiota Transplantation (FMT) Mechanical interest in immune-mediated ocular disease Not standard care; safety and donor selection issues
Metabolite therapy Targets SCFAs, bile acids or tryptophan pathways Early research

Limitations of Current Evidence

  • Many studies are cross-sectional and cannot prove causality.
  • Results are influenced by diet, age, geography, systemic disease, medications and sequencing methods.
  • Taxonomic findings may not reflect functional microbial activity.
  • Animal and human microbiome findings may not translate directly.
  • Microbiome-targeted ocular therapies require disease-specific randomised trials.

Future research direction

There is a recognized link between gut microbiota and immune-related diseases. Future studies should aim to clarify how gut commensal bacteria contribute to sustaining the host’s immune equilibrium. Patients with uveitis experience changes in gut fungal diversity, indicating that treatments such as fecal microbiota transplantation (FMT) need to address the entire gut microbiome rather than just bacteria. Because gut bacteria interact dynamically and cooperatively, multi-strain probiotic blends may provide more effective and lasting therapeutic outcomes. Identifying prebiotic compounds that work well, establishing their best dosage and delivery methods, and confirming their clinical effectiveness will be crucial tasks for upcoming research.[6]

  • Future research should move beyond cross-sectional association studies toward longitudinal, mechanistic, and interventional designs.
  • Key priorities include identifying disease-specific microbial signatures, defining functional microbial metabolites, standardising sequencing and bioinformatics methods, accounting for diet and medication confounders, and validating findings across diverse populations.
  • Clinical trials are needed to determine whether microbiome-targeted interventions such as diet modification, prebiotics, probiotics, synbiotics, metabolite-based therapy, or fecal microbiota transplantation can meaningfully alter ocular disease activity or progression.
  • As probiotic effects are highly strain-specific, future studies should define the exact strain, dose, duration, safety profile, and target disease phenotype.

Clinical Takeaways

  • The gut-eye axis is an emerging framework linking intestinal dysbiosis with ocular inflammation, retinal degeneration, vascular dysfunction, and ocular surface disease.
  • Current evidence is strongest for associations in uveitis, AMD, dry eye/Sjogren’s syndrome, and some retinal vascular disorders, but causality remains incompletely proven.
  • Microbiome findings are influenced by diet, age, geography, systemic disease, medications, and sequencing methodology.
  • Microbiome testing is not currently part of routine ophthalmic evaluation.
  • Microbiome-targeted therapies are promising but remain investigational and should not replace standard ophthalmic care.

References

  1. ↑ Cavuoto, Kara M., et al. “Relationship between the Microbiome and Ocular Health.” The Ocular Surface, vol. 17, no. 3, 2019, pp. 384–392., https://doi.org/10.1016/j.jtos.2019.05.006.
  2. ↑ Zheng W, Su M, Hong N, Ye P. Gut-eye axis. Adv Ophthalmol Pract Res. 2025 Jan 27;5(3):165-174. doi: 10.1016/j.aopr.2025.01.003. PMID: 40567942; PMCID: PMC12192331.
  3. ↑ Nguyen Y, Rudd Zhong Manis J, Ronczkowski NM, Bui T, Oxenrider A, Jadeja RN and Thounaojam MC (2024) Unveiling the gut-eye axis: how microbial metabolites influence ocular health and disease. Front. Med. 11:1377186. doi: 10.3389/fmed.2024.1377186
  4. ↑ 4.0 4.1 Wang C, Li H, Wang T, Li X, Liu J, Deng A, Jiao X. The gut-eye axis in blinding eye diseases: microbiota-driven immune dysregulation and immunomodulatory therapies. Int Ophthalmol. 2025 Dec 29;46(1):57. doi: 10.1007/s10792-025-03921-8. PMID: 41460363.
  5. ↑ Zhao Y, Qiu P, Shen T. Gut microbiota and eye diseases: A review. Medicine (Baltimore). 2024 Sep 27;103(39):e39866. doi: 10.1097/MD.0000000000039866. PMID: 39331938; PMCID: PMC11441905.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Priyanka P, Khullar S, Singh M, Morya AK, Sharma B, Periasamy B, Moharana B, Morya R. Role of gut microbiomes in different ocular pathologies: A systematic review. World J Gastrointest Pathophysiol 2025; 16(4): 113488 [PMID: 41479867 DOI: 10.4291/wjgp.v16.i4.113488]                
  7. ↑ 7.0 7.1 7.2 Manor, Ohad, et al. “Health and Disease Markers Correlate with Gut Microbiome Composition across Thousands of People.” Nature Communications, vol. 11, no. 1, 2020, https://doi.org/10.1038/s41467-020-18871-1.
  8. ↑ Shabani M, Ghoshehy A, Mottaghi AM, Chegini Z, Kerami A, Shariati A and Taati Moghadam M (2025) The relationship between gut microbiome and human diseases: mechanisms, predisposing factors and potential intervention. Front. Cell. Infect. Microbiol. 15:1516010. doi: 10.3389/fcimb.2025.1516010
  9. ↑ Kammoun S, Rekik M, Dlensi A, Aloulou S, Smaoui W, Sellami S, Trigui K, Gargouri R, Chaari I, Sellami H, Elatoui D, Khemakhem N, Hadrich I, Neji S, Abdelmoula B, Bouayed Abdelmoula N. The gut-eye axis: the retinal/ocular degenerative diseases and the emergent therapeutic strategies. Front Cell Neurosci. 2024 Sep 26;18:1468187. doi: 10.3389/fncel.2024.1468187. PMID: 39391760; PMCID: PMC11464360.
  10. ↑ Szymańska K, et al. The Gut-Eye Axis and Microbiome in Ophthalmic Diseases. 2026J. Clin. Med. 2026, 15(10), 3563; https://doi.org/10.3390/jcm15103563
  11. ↑ Zhuang, He, et al. “Dysbiosis of the Gut Microbiome in Lung Cancer.” Frontiers in Cellular and Infection Microbiology, vol. 9, no. 18 Apr. 2019, https://doi.org/10.3389/fcimb.2019.00112.
  12. ↑ 12.0 12.1 12.2 Carding, Simon, et al. “Dysbiosis of the gut microbiota in disease.” Microbial Ecology in Health and Disease, vol. 26, no. 1, 2015, DOI: 10.3402/mehd.v26.26191
  13. ↑ Marietta, Eric, et al. “Intestinal Dysbiosis in, and Enteral Bacterial Therapies for, Systemic Autoimmune Diseases.” Frontiers in Immunology, vol. 11, 2020, https://doi.org/10.3389/fimmu.2020.573079.
  14. ↑ Hevia, Milani, et al. “Intestinal dysbiosis associated with systemic lupus erythematosus.” mBio, vol. 5, 2014, doi: 10.1128/mBio.01548-14.
  15. ↑ Marc Labetoulle, Christophe Baudouin, Jose M. Benitez del Castillo, Maurizio Rolando, Maria Rescigno, Elisabeth M. Messmer, Pasquale Aragona,How gut microbiota may impact ocular surface homeostasis and related disorders,Progress in Retinal and Eye Research,Volume 100,2024,101250,ISSN 1350 -9462,https://doi.org/10.1016/j.preteyeres.2024.101250
  16. ↑ Gal Antman, Lukas Ritzer, Anat Galor, Alice Verticchio Vercellin, Brent A. Siesky, Denise Alabi, Jason Vayner, Fani Segev, Alon Harris,The relationship between dry eye disease and human microbiota: A review of the science Experimental Eye Research,Volume 245,2024,109951,ISSN 0014-4835, https://doi.org/10.1016/j.exer.2024.109951.
  17. ↑ Frizon L, Rocchetti TT, Frizon A, de Alcântara RJA, de Paiva CS, Gomes JÁP. The Gut Microbiome in Stevens-Johnson Syndrome and Sjögren's Disease: Correlations with Dry Eye. Microorganisms. 2025 Nov 29;13(12):2730. doi: 10.3390/microorganisms13122730. PMID: 41471933; PMCID: PMC12735903.
  18. ↑ Rajagopalaboopathi Jayasudha, Sama Kalyana Chakravarthy, Gumpili Sai Prashanthi, Savitri Sharma, Mudit Tyagi, Sisinthy Shivaji; Implicating Dysbiosis of the Gut Fungal Microbiome in Uveitis, an Inflammatory Disease of the Eye. Invest. Ophthalmol. Vis. Sci. 2019;60(5):1384-1393. https://doi.org/10.1167/iovs.18-26426.
  19. ↑ Samalia PD, Solanki J, Kam J, Angelo L, Niederer RL. From Dysbiosis to Disease: The Microbiome's Influence on Uveitis Pathogenesis. Microorganisms. 2025 Jan 25;13(2):271. doi: 10.3390/microorganisms13020271. PMID: 40005638; PMCID: PMC11857511.
  20. ↑ Gao Q, Xiong M, Zhou S, Lu J, Ren B, Peng Q, Zeng M and Song H (2026) Gut microbiota and uveitis: exploring novel mechanisms of inflammatory ocular diseases via the gut-eye axis. Front. Microbiol. 17:1749111. doi: 10.3389/fmicb.2026.1749111
  21. ↑ Schiavone N, Isoldi G, Calcagno S, Rovida E, Antiga E, De Almeida CV, Lulli M. Exploring the Gut Microbiota-Retina Axis: Implications for Health and Disease. Microorganisms. 2025 May 10;13(5):1101. doi: 10.3390/microorganisms13051101. PMID: 40431274; PMCID: PMC12113749.
  22. ↑ Chang YH, Yeh YM, Lee CC, Chiu CH, Chen HC, Hsueh YJ, Lee CW, Lien R, Chu SM, Chiang MC, Kang EY, Chen KJ, Wang NK, Liu L, Hwang YS, Lai CC, Wu WC. Neonatal gut microbiota profile and the association with retinopathy of prematurity in preterm infants. Clin Exp Ophthalmol. 2025 Jan-Feb;53(1):54-66. doi: 10.1111/ceo.14441. Epub 2024 Sep 25. PMID: 39322810.
  23. ↑ Zhou B, Parekh Z, Phung C, Rodriguez SH, Skondra D. The gut-retina axis in age-related macular degeneration: immune crosstalk and metabolite production. Exp Biol Med (Maywood). 2026 Feb 23;251:10847. doi: 10.3389/ebm.2026.10847. PMID: 41809655; PMCID: PMC12968045.
  24. ↑ Berkowitz E, Kopelman Y, Kadosh D, Carasso S, Tiosano B, Kesler A, Geva-Zatorsky N. "More Guts Than Brains?"-The Role of Gut Microbiota in Idiopathic Intracranial Hypertension. J Neuroophthalmol. 2022 Mar 1;42(1):e70-e77. doi: 10.1097/WNO.0000000000001330. Epub 2021 Jul 13. PMID: 34270519.
  25. ↑ Omar WEW, Singh G, McBain AJ, Cruickshank F, Radhakrishnan H. Gut Microbiota Profiles in Myopes and Nonmyopes. Invest Ophthalmol Vis Sci. 2024 May 1;65(5):2. doi: 10.1167/iovs.65.5.2. PMID: 38691091; PMCID: PMC11077909.
  26. ↑ Ullah Z, Tao Y, Mehmood A, Huang J. The Role of Gut Microbiota in the Pathogenesis of Glaucoma: Evidence from Bibliometric Analysis and Comprehensive Review. Bioengineering (Basel). 2024 Oct 24;11(11):1063. doi: 10.3390/bioengineering11111063. PMID: 39593723; PMCID: PMC11591249.
  27. ↑ Lujia Zhou, Yan Ma, Xiumiao Li, Guofan Cao, Gut-eye axis in ophthalmic diseases: Focus on ocular neurodegeneration,Biomedicine & Pharmacotherapy,Volume 193,2025,118800,ISSN 0753-3322,https://doi.org/10.1016/j.biopha.2025.118800
  28. ↑ Songel-Sanchis B, Morales-Fernández L, García-Bardera J, Güemes-Villahoz N, Martínez-de-la-Casa JM, García-Feijoo J. The Ocular and Gut Microbiome Axis in Understanding Glaucoma: A Systematic Review. J Clin Med. 2026 Feb 4;15(3):1245. doi: 10.3390/jcm15031245. PMID: 41682924; PMCID: PMC12898600.
  29. ↑ Wu Y, Shi R, Chen H, Zhang Z, Bao S, Qu J, et al. Effect of the gut microbiome in glaucoma risk from the causal perspective. BMJ Open Ophthalmology. 2024;9:e001547. https://doi.org/10.1136/bmjophth-2023-001547
  30. ↑ Zhao, X., Ren, Z., Li, W. et al. Alterations in ocular fungal microbiota in patients with fungal keratitis: a comparative study from coastal regions of Eastern China. BMC Ophthalmol 25, 316 (2025). https://doi.org/10.1186/s12886-025-04133-5
  31. ↑ Kalyana Chakravarthy S, Jayasudha R, Ranjith K, Dutta A, Pinna NK, Mande SS, Sharma S, Garg P, Murthy SI, Shivaji S. Alterations in the gut bacterial microbiome in fungal Keratitis patients. PLoS One. 2018 Jun 22;13(6):e0199640. doi: 10.1371/journal.pone.0199640. Erratum in: PLoS One. 2019 Jan 30;14(1):e0211757. doi: 10.1371/journal.pone.0211757. PMID: 29933394; PMCID: PMC6014669.
  32. ↑ Berzack S, Galor A. Microbiome-based therapeutics for ocular diseases. Clin Exp Optom. 2025 Mar;108(2):115-122. doi: 10.1080/08164622.2024.2422479. Epub 2024 Dec 1. PMID: 39617011; PMCID: PMC11875938.
  33. ↑ Watane A, Cavuoto KM, Rojas M, Dermer H, Day JO, Banerjee S, Galor A. Fecal Microbial Transplant in Individuals With Immune-Mediated Dry Eye. Am J Ophthalmol. 2022 Jan;233:90-100. doi: 10.1016/j.ajo.2021.06.022. Epub 2021 Jun 30. PMID: 34214453; PMCID: PMC8678170.
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