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Gut microbiota disorders and ophthalmic diseases Cover
Open Access
|Mar 2026

Abstract

Introduction

The intestinal microbiota is one of the key elements in maintaining human homeostasis. Disruption of its balance, known as dysbiosis, is now increasingly implicated as a contributing factor for many diseases, including ophthalmic conditions.

Materials and methods

This review synthesizes a current literature review 2020–2025 addressing the relationship between the interplay between gut microbiota dysbiosis and major ophthalmic disorders, notably age-related macular degeneration (AMD), retinopathy of prematurity (ROP), glaucoma, diabetic retinopathy (DR), and autoimmune uveitis.

Results

Potential pathogenic mechanisms are discussed, including compromised intestinal barrier integrity, aberrant immune activation, the presence of bacterial endotoxins (e.g., LPS), and the influence of microbially derived metabolites on the gut–retina axis. Particular emphasis is placed on the roles of Th17 and Treg cells, inflammatory cytokines, and the importance of short-chain fatty acids (SCFAs), among other bioactive molecules. The significance of the neonatal microbiome and its influence on the development of ophthalmic diseases in premature infants is also highlighted.

Conclusions

Gut microbiota dysregulation may represent a key contributor in the development and progression of several ophthalmic conditions. The microbiota–gut–retina axis represents an emerging and promising therapeutic target for future research and therapies. Integrating microbiota-targeted interventions may significantly improve treatment outcomes and quality of life for ophthalmic patients.

DOI: https://doi.org/10.21164/pomjlifesci.1140 | Journal eISSN: 2719-6313 | Journal ISSN: 2450-4637
Language: English
Page range: 16 - 21
Published on: Mar 3, 2026
In partnership with: Paradigm Publishing Services
Publication frequency: 4 issues per year

© 2026 Wiktoria Bosy-Gąsior, Monika Modrzejewska, published by Pomeranian Medical University
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.