Soundharya S, BSc. Clinical Nutrition and Dietetics

MMM College of Health Sciences, Chennai, India



The commensal micro-organisms that reside normally on the human body and their genetic material are collectively known as the human microbiome.(1) The vast majority of them reside in the gastrointestinal tract. The GI tract is composed of 100 trillion micro-organisms that coexist in a symbiotic relation with the host and influence an array of bodily functions, including metabolic processes and 70% of the body’s immune system. (2)



What is Gut dysbiosis?

The composition of the gut microbiome is determined by many factors including genetics, disease, diet, and medication with diet quality considered a particularly strong factor.(3) Dysbiosis is defined as a shift or change in the composition of the microbiome. A high-fat and glycaemic index diet results in gut barrier dysfunction which increases intestinal permeability and promotes pro-inflammatory gut microbiota.(3,4) When dysbiosis occurs, a disruption in the homeostatic state can potentiate growth and invasion of pathogenic species. Gut dysbiosis has been implicated in eye diseases such as dry eye, uveitis, diabetic retinopathy, glaucoma, and age-related macular degeneration. (5)

Autoimmune Uveitis (6)

  • Autoimmune uveitis is a sterile inflammatory disorder affecting the retina and uvea (choroid, iris, and ciliary body).
  • The disease is thought to be driven by infiltration of inflammatory cells and activation of auto-reactive T cells that can respond to retinal proteins.
  • The activated T cell was present in the dysbiotic gut before disease in the retina was apparent.
  • This suggests that gut commensals are required for the activation of autoreactive T cells implying the contribution of gut microbes in triggering uveitis.
  • The inflammation at the intestinal mucosa may increase gut permeability and facilitate the translocation of microbes (or microbial by products) that incite ocular inflammation, either through direct effects on the eyes or indirectly via molecular mimicry and immune sensitization.
  • Exogenous administration of short chain fatty acids (SCFAs), which are intestinal bacteria-derived fermentation metabolites of dietary fibre, can reduce the severity of uveitis through two mechanisms, by enhancing Tregs in the colon and cervical lymph nodes, and by reducing the trafficking of effector T cells between the intestines and the spleen during uveitis.

Age-Related Macular Degeneration (AMD) (7)

  • AMD is characterized by retinal pigmented epithelial cell dysfunction and choroidal neovascularization.
  • Alterations in the intestinal microbiota are relevant to pathogenesis of AMD that results in altering the fatty acid metabolism and carotenoid biosynthesis pathway.
  • High-fat diet, which accompanies gut dysbiosis, can induce retinal inflammation and increased plasma IL-6, IL-1b, tumour necrosis factor (TNF)-α, and vascular endothelial growth factor, inducing choroidal angiogenesis.
  • A high glycaemic diet resulted in gut dysbiosis that were associated with AMD-like features such as retinal pigment epithelium (RPE) atrophy, lipofuscin accumulation, and photoreceptor atrophy.

Primary open angle glaucoma (POAG) (8)

  • Glaucoma is defined as an optic neuropathy related to an increase in intraocular pressure (IOP) and alteration of drainage of aqueous humour in the anterior chamber of the eye. In open-angle glaucoma, an open drainage method is not sufficient to maintain normal IOP.
  • A healthy gut microbiota could promote the production of neuroprotective factors that in turn promote the survival of retinal ganglion cells.
  • Helicobacter pylori, a non-commensal colonizer of the gastrointestinal tract affects the IOP and visual field measurements.
  • Pylori increases the risk of glaucoma through the effect of reactive oxygen species and inflammatory cytokines that may travel from the gastric mucosa to the optic disc which causes glaucomatous changes in the globe.
  • Toxins of H. pylori may influence the glaucoma and cause antibody-induced apoptosis, which is attributed to inflammation in the retrobulbar area.

Foods to embrace on (9)

  • Probiotics – Curd, yogurt, fermented rice, sauerkraut, kimchi, and kefir.
  • Prebiotics – Green leafy vegetables, spinach, Tomatoes, artichokes, bananas, asparagus, berries, garlic, onions, chicory, green vegetables, legumes, as well as oats, linseed, barley, and wheat.



  1. Lin, P. (2018). The role of the intestinal microbiome in ocular inflammatory disease. Current opinion in ophthalmology29(3), 261-266.
  2. John, G. K., & Mullin, G. E. (2016). The gut microbiome and obesity. Current oncology reports18(7), 1-7
  3. Jamar, G., Ribeiro, D. A., & Pisani, L. P. (2021). High-fat or high-sugar diets as trigger inflammation in the microbiota-gut-brain axis. Critical reviews in food science and nutrition61(5), 836-854.
  4. Bibbò, S., Ianiro, G., Giorgio, V., Scaldaferri, F., Masucci, L., Gasbarrini, A., & Cammarota, G. (2016). The role of diet on gut microbiota composition. Eur Rev Med Pharmacol Sci20(22), 4742-4749.
  5. Singh, R. K., Chang, H. W., Yan, D. I., Lee, K. M., Ucmak, D., Wong, K., … & Liao, W. (2017). Influence of diet on the gut microbiome and implications for human health. Journal of translational medicine15(1), 1-17.
  6. Zárate-Bladés, C. R., Horai, R., & Caspi, R. R. (2016). Regulation of Autoimmunity by the Microbiome. DNA and cell biology35(9), 455-458.
  7. Lin, P. (2019). Importance of the intestinal microbiota in ocular inflammatory diseases: A review. Clinical & experimental ophthalmology47(3), 418-422.
  8. Baim, A. D., Movahedan, A., Farooq, A. V., & Skondra, D. (2019). The microbiome and ophthalmic disease. Experimental Biology and Medicine244(6), 419-429.
  9. Markowiak, P., & Śliżewska, K. (2017). Effects of probiotics, prebiotics, and synbiotics on human health. Nutrients9(9), 1021.