The Gut–Eye Axis: Probiotics, Metabolites, and Intraocular Pressure

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The Gut–Eye Axis and Ocular HealthThe emerging concept of a gut–eye axis recognizes that gut microbes and their products can affect the eye. Gut bacteria ferment fibers to produce short-chain fatty acids (SCFAs) (like acetate, propionate, butyrate) and modify bile acids (BAs). These metabolites enter the circulation and can reach the eye, influencing its immune environment and function (). For example, microbial dysbiosis – an imbalance in gut flora – has been linked to ocular diseases from age-related macular degeneration and uveitis to dry eye and glaucoma (). In fact, a recent survey found that gut imbalance is associated with multiple eye conditions, and only a handful of early trials (four of 25 studies) have tested interventions like probiotics or fecal transplants on eye disease (). This gut–eye axis suggests that gut-derived SCFAs, BAs, and even inflammatory components (like LPS) could modulate ocular immune tone (the baseline immune status) and affect tissues like the trabecular meshwork (the fluid drainage filter) and intraocular pressure (IOP).Microbial Metabolites and Ocular ImmunityShort-Chain Fatty Acids (SCFAs)SCFAs are fatty acids with fewer than six carbon atoms, mainly acetate, propionate, and butyrate, produced by gut bacteria digesting fiber. They regulate immune responses systemically () (). In the eye, SCFAs exert anti-inflammatory effects. In mouse models, injected SCFAs were detected in ocular tissues and reduced inflammation from endotoxin (LPS) exposure () (). This shows SCFAs can cross the blood–eye barrier via blood and calm intraocular inflammation. For instance, intraperitoneal butyrate in mice dampened LPS-induced uveitis, reducing pro-inflammatory cytokines and boosting regulatory T cells () (). Likewise, a review notes SCFAs attenuate ocular inflammation after systemic injection (). These anti-inflammatory actions imply SCFAs help maintain a healthy ocular immune tone (keeping immune activity in check). In contrast, gut-derived pro-inflammatory signals can harm the eye. Gut bacteria (especially Gram-negative) release LPS which triggers innate immune receptors like TLR4. TLR4 signaling is known to affect the trabecular meshwork and has been genetically linked to primary open-angle glaucoma (). In animals, giving LPS worsens retinal neuronal loss and photoreceptor damage (). Thus, a balanced gut flora (with abundant SCFA-producers) supports eye health, while dysbiosis may flood the eye with inflammatory signals.Bile AcidsBile acids (BAs) are cholesterol-derived compounds made by the liver and modified by gut microbes. Aside from digesting fats, BAs are signaling molecules with anti-inflammatory and neuroprotective roles (). Emerging evidence highlights BAs’ benefits in retinal and ocular disorders. For example, ursodeoxycholic acid (UDCA) and its taurine-conjugate TUDCA have shown protective effects in diabetic retinopathy and macular degeneration models (). In mouse diabetic retinopathy models, UDCA treatment restored the blood-retinal barrier and sharply reduced retinal inflammation (lowering IL-1β, IL-6) (). UDCA also preserved capillary integrity and reduced cell loss in the retina (). Moreover, systemic UDCA or TUDCA suppressed aberrant blood vessel growth (choroidal neovascularization) in ocular injury models (). Mechanistically, BAs act via receptors like FXR and TGR5. In experimental uveitis, low BA levels were found, and restoring BAs (through TGR5 signaling) dampened NF-κB activation in immune cells (). Thus, gut-derived BAs c